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OBJECTIVES: To evaluate the effect of small-group education including practical training on dental students' shade determination performance compared with a control group. METHODS: Sixty-three non-colour-blind preclinical students were asked to participate and belonged to an intervention (n = 31) and a control (n = 32) group, respectively. All students received a lecture on dental shade determination. The members of the intervention group were educated and practically trained in small groups in addition. Ten volunteers, each with unrestored upper right middle and lateral incisors, were recruited. The students of both the intervention and control groups were then asked to determine the colour of the volunteers' test teeth using the 3D-Master shade guide (Vita Zahnfabrik, Bad Säckingen, Germany) under artificial daylight illumination. For analytical purposes, the CIE L*a*b* coordinates were obtained using a spectrophotometer. Colour differences, ΔE, between all shade tabs selected by the students and the natural teeth were calculated. ΔE observed in the intervention and control groups were compared using t tests. In addition, a multi-level regression model was adjusted for age and gender. RESULTS: Mean (SD) ΔE between the shade tabs selected by the students and the natural teeth in the intervention and control groups were 3.8 (2.1) and 4.3 (2.3), respectively (P < .001). The effect of group membership was reproduced in multivariate analysis whereas age and gender did not reach statistical significance. CONCLUSIONS: With more intensive education and practical training the ability to perform clinical shade determinations improved for students without previous clinical experience. The results obtained support the idea of implementing thematic small-group education in the dental curriculum.

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The purpose of this study was to measure enamel wear caused by antagonistic monolithic zirconia crowns and to compare this with enamel wear caused by contralateral natural antagonists. Twenty monolithic zirconia full molar crowns were placed in 20 patients. Patients with high activity of the masseter muscle at night (bruxism) were excluded. For analysis of wear, vinylpolysiloxane impressions were prepared after crown incorporation and at 6-, 12-, and 24-month follow-up. Wear of the occlusal contact areas of the crowns, of their natural antagonists, and of two contralateral natural antagonists (control teeth) was measured by use of plaster replicas and a 3D laser-scanning device. Differences of wear between the zirconia crown antagonists and the control teeth were investigated by means of two-sided paired Student's t-tests and linear regression analysis. After 2 years, mean vertical loss was 46 µm for enamel opposed to zirconia, 19-26 µm for contralateral control teeth and 14 µm for zirconia crowns. Maximum vertical loss was 151 µm for enamel opposed to zirconia, 75-115 µm for control teeth and 60 µm for zirconia crowns. Statistical analysis revealed significant differences between wear of enamel by zirconia-opposed teeth and by control teeth. Gender, which significantly affected wear, was identified as a possible confounder. Monolithic zirconia crowns generated more wear of opposed enamel than did natural teeth. Because of the greater wear caused by other dental ceramics, the use of monolithic zirconia crowns may be justified.

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The purpose of this study was to evaluate enamel wear caused by monolithic zirconia crowns and to compare this with enamel wear caused by contralateral natural antagonists. Twenty monolithic zirconia crowns were placed in 20 patients requiring full molar crowns. For measurement of wear, impressions of both jaws were made at baseline after crown cementation and at 6-month follow-up. Mean and maximum wear of the occlusal contact areas of the crowns, of their natural antagonists and of the two contralateral natural antagonists were measured by the use of plaster replicas and 3D laser scanning methods. Wear differences were investigated by the use of two-sided paired Student's t-tests and by linear regression analysis. Mean vertical loss (maximum vertical loss in parentheses) was 10 (43) µm for the zirconia crowns, 33 (112) µm for the opposing enamel, 10 (58) µm for the contralateral teeth and 10 (46) µm for the contralateral antagonists. Both mean and maximum enamel wear were significantly different between the antagonists of the zirconia crowns and the contralateral antagonists. Gender and activity of the masseter muscle at night (bruxism) were identified as possible confounders which significantly affected wear. Under clinical conditions, monolithic zirconia crowns seem to be associated with more wear of opposed enamel than are natural teeth. With regard to wear behaviour, clinical application of monolithic zirconia crowns is justifiable because the amount of antagonistic enamel wear after 6 months is comparable with, or even lower than, that caused by other ceramic materials in previous studies.

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The purpose of this prospective cohort study was to assess the performance of tooth-supported, extended zirconia, fixed dental prostheses (FDPs). Thirty FDPs with span-lengths between 36 and 46 mm (mean: 40.33 mm), four to seven units and with connector dimensions of approximately 9 mm(2) were inserted (19 in the posterior region, 11 including anterior teeth) using glass-ionomer cement and assessed (aesthetic evaluation, failures, hypersensitivity/tooth vitality, secondary caries, pocket depth, decementation and chipping) at baseline and after 2 years. Differences between baseline and 2-year recall were analysed using the Wilcoxon signed-rank test for matched pairs. There were five failures. One FDP revealed a core fracture at the base of the connector, probably caused by a damage induced during fabrication. Two FDPs had to be recemented, one abutment tooth had to be treated endodontically and one cohesive failure of the veneer was observed. There were no significant changes of pocket depth and hypersensitivity between baseline and 2-year recall. The aesthetics were rated as excellent by the patients at both baseline and recall. Two year clinical results of extended zirconia based FDPs with 9 mm(2) connectors are promising.

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OBJECTIVES: The aim of the investigation was to examine the color stability of seven resin-based facing composites with a high content of inorganic filling material (Colombus, Artglass, Sinfony, Targis, Zeta LC, Zeta HC, BelleGlass HP/dentine, BelleGlass HP/enamel). METHODS: Changes in color of test samples were determined after UV irradiation in a fast-action UV instrument, Sunset CPS+, and after storage in a mouthrinse, tea, coffee, red wine and a 0.1% turmeric (curcuma) solution. Color differences were measured by using a Castor colorimeter and the total amount of color difference represented as DeltaE. RESULTS: Red wine and the turmeric solution caused the most severe cases of discoloration (DeltaE>10). Tea, coffee, the mouthrinse and UV irradiation caused invisible (DeltaE<1) or visible (DeltaE>1), and to some extent clinically unacceptable (DeltaE>3.3), discoloration. SIGNIFICANCE: It is apparent from the results that it remains essential to improve the color stability of the composite resin materials used for facings.

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Since the detection of vitamin E in 1922, nearly 50 years passed until the recognition that there is a pathogenic vitamin E deficiency in humans. Such a deficiency can be found mostly in a disturbed resorption or transport of the vitamin (mucoviscidosis, chronic cholestasis, abetalipoproteinaemia) and leads typically to a progredient spinocerebellar ataxia in combination with a polyneuropathy. Substitution of the vitamin may hinder a further progression or even lead to an amelioration of the symptoms. Prophylactic treatment in abetalipoproteinaemia prevents the otherwise unavoidable neurological deficits. Isolated vitamin E deficiency is a rare syndrome and the causes are still obscure. We observed a 26 year old male patient with such a isolated vitamin E deficiency who was hitherto thought to suffer from Friedreich's ataxia. The clinical feature showed in addition to the "classical" symptoms of vitamin E deficiency cranial nerve involvement, perioral dystonia and pyramidal signs. Histologically (M. gastrocnemius) we saw the described typical but not specific changes (neurogenic atrophy, phosphatase-positive vacuoles with myelin bodies, cores). An oral vitamin E resorption test yielded a very shortened serum half life. These results support the hypothesis that in the pathophysiology of isolated vitamin E deficiency malelimination plays an important role in addition the known malresorptions models.

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We examined the time course of CK and its isoenzymes in 15 patients with severe ischemic stroke. Patients with cerebral transtentorial herniation (n = 7) had the highest CK-BB activity during herniation (1.54 +/- 0.6 U/L, mean +/- SD; range: 1.0-2.6 U/L). These values were distinctly above the values of a control group of 20 patients with non-neurological diseases (0.39 +/- 0.2 U/L, mean +/- SD). In patients with smaller lesions without herniation (n = 8) the maximum CK-BB increase was lower (0.56 +/- 0.26 U/L, mean +/- SD).

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The possible relationship between plasma renin activity and neurological deficits was examined in ten patients with spontaneous subarachnoid haemorrhage in a prospective clinical study. The patients were examined daily, particular attention being given to signs of brain stem dysfunction. The degree of impaired consciousness was assessed using the Glasgow Coma Score. Plasma renin activity was determined on days 1-5, 7, 9, 11, 13, 15 and 21 after the initial bleeding episode using an Angiotensin-I-radioimmunoassay. Six of seven patients with signs of brain stem dysfunction displayed a marked increase in plasma renin activity. Thus a significant negative correlation between the degree of consciousness and the plasma renin activity resulted. An explanation for this correlation may be found in the localization of the autonomous centres and the high concentrations of renin in the hypothalamus and brain stem. The individual changes in plasma renin activity have prognostic significance, whereas single estimated plasma renin activities show great inter-individual differences and have only limited prognostic value.

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Neurogenically caused cardiac arrhythmias and their correlation to lesions within the central nervous system were examined prospectively in 54 patients with spontaneous intracerebral hemorrhage. All patients were examined neurologically daily for 3 weeks, with special attention given to signs of brainstem compression resulting from transtentorial herniation. Electrocardiograms were continuously recorded over an average of 5 days. A significant correlation was established between the clinical manifestations of brainstem compression and sinus arrhythmias, multifocal premature ventricular contractions, couplets, and ventricular tachycardias. An explanation for this correlation may be found in the localization of the autonomous cardiovascular centers in the hypothalamus and brainstem. Transtentorial herniation frequently leads to a bilateral lesion of these structures. However, the cardiac arrhythmias are only a partial phenomenon within a complex cardiovascular reaction.

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There have been no reports of studies on nocturnal sleep or quantitative studies of sleep spindle density in Huntington's disease, whereas sleep in Parkinson's disease has been extensively reported. We therefore examined nocturnal sleep changes in patients with Parkinson's and Huntington's disease and compared them with a control group. The previously reported decrease in sleep spindle density was observed in patients with Parkinson's disease. The patients with Huntington's disease, however, had a significant increase in sleep spindle density, the nocturnal sleep pattern being normal in other respects when compared with the control group. This observation may provide a further diagnostic criterion in Huntington's disease.

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In this prospective study 52 patients with spontaneous subarachnoid haemorrhage were examined with respect to cardiac arrhythmias and their relationship to cerebral lesions. A continuous ECG was registered over an average of five days. Sinus tachycardia was the most frequently recorded arrhythmia, followed by multifocal ventricular extrasystoles, couplets, frequent supraventricular extrasystoles, non-sustained ventricular tachycardia, asystolia and sinus arrhythmia. A significant correlation was found between the clinical manifestation of a midbrain syndrome and sinus arrhythmia, and multifocal ventricular extrasystoles. This correlation points to the autonomic cardiovascular centres as the structures involved.

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In 154 patients with spontaneous subarachnoid hemorrhage owing to a ruptured aneurysm, the way by which the diagnosis was arrived at was checked. The correct diagnosis was missed initially in 52 patients (33.8%) and the subarachnoid hemorrhage was misinterpreted most frequently as systemic infection, brain tumor, disorder of cerebral blood flow or cervical spinal syndrome. The proportion of false diagnosis was especially high in younger patients with an initially less severe illness. Freely practicing physicians without specialist neurological training missed the diagnosis in 33.3%, free practicing specialists for nervous diseases and neurologists in 17.4%, doctors at smaller hospitals in 16.3% and doctors at the Neurologic Division, University Hospital for Nervous Diseases in Homburg/Saar in 6.5%. The time up to correction of a wrong initial diagnosis was up to seven days in 34 patients (65.4%), up to 14 days in 13 patients (25.0%) and between 15 and 27 days in five patients (9.6%).

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Neurogenic cardiac arrhythmias during 5 cases of subarachnoid rebleeding in 4 patients were analyzed by using long-term ECG (Holter). The initial onset of rebleeding was characterized by an abrupt decrease of heart rate from 93.3 +/- 7.85 (beats/min) to 63.3 +/- 14.6 (beats/min). This was immediately followed by pronounced tachycardia of 163.0 +/- 20.9 (beats/min) and subsequently, alterations of the P wave, ST depression with an increase in T wave amplitude. Frequent premature ventricular contractions, couplets, and self-terminating episodes of ventricular tachycardia for 2-8 minutes were observed during 2 episodes of rebleeding, an idioventricular rhythm in one case. The ECG returned to normal in the 3 non-lethal cases. Pathogenetically, the initial heart rate decrease with varying P wave configuration can be explained through activation of the baroreceptor reflex. Elevated intracranial pressure causes a blood pressure increase thus stimulating the baroreceptors and consequently, the afferent and efferent tracts of the vagus nerve. The sympathicotonus appears to have a modulating effect.

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