Dental implants placed by undergraduate students: clinical outcomes and patients'/students' perceptions.

INTRODUCTION: Implant dentistry in undergraduate education is predominantly theoretical or prosthetics oriented. Clinical experience with implant surgery could provide students a better understanding of alternatives for tooth replacements. This study describes an implant dentistry programme for undergraduate students, which included surgical placement of implants. The study presents the clinical outcomes of the programme, patients' satisfaction and students' attitudes/perceptions. It reflects on barriers and problems encountered during implementation and provides suggestions for other institutions. MATERIALS AND METHODS: Thirty-six students placed one implant each for a single tooth replacement after careful radiographic assessment and pre-surgical planning. One-stage surgery was performed under one-to-one supervision. Crowns were cemented on individual abutments 3-6 months later. Crestal bone loss was assessed radiographically immediately after surgery, at crown placement and after 1 year of loading. Questionnaires were used to investigate patients' perspectives and students' opinions towards the programme, as well as their perceived level of competence. RESULTS: Thirty-six implants were placed in 27 patients; two (5.6%) failed prior to loading; mean bone loss from time of surgery to crown placement was 1.41 mm and remained unchanged thereafter, reflecting implant success. Overall, patients were satisfied and the majority would repeat the treatment by a student. The students thought it was a valuable experience, although they realised that additional education is necessary to perform implant surgery without supervision. CONCLUSION: Implant placement by undergraduate students resulted in acceptable clinical outcome parameters, patient satisfaction and positive student perceptions. These findings support the further development of clinical implant education in undergraduate dental curricula.

[Implementation of computerized phisician order entry in a hospital setting: what are the keys to success?]. / Implémentation de la prescription informatisée en milieu hospitalier: quelles sont les clés d'un déploiement réussi ?

INTRODUCTION: A software of computerized physician order entry [CPOE] was developed by a data-processing company in collaboration with the Mont-Godinne University Hospital By 2006, parallel to the evolution of the software, the progressive implementation of CPOE was carried out, and currently covers 16 wards, the emergency room, the recovery rooms and the center of medical care [day hospital] as well as the day surgical center OBJECTIVES: Complete computerization of the drug supply chain, including the regulation by the physician, the pharmaceutical validation, the delivery and the follow-up of stocks by pharmacy, the validation of the administration by the nurse and the tariffing of the drugs. METHOD AND RESULTS: In 2006, a working group was created in order to validate specifications allowing the development of a software of CPOE, Linked to the computerized medical record. A data-processing company was selected in order to develop this software. Two beds were computerized in the pneumology ward, in order to test and validate the software. From 2007 to 2009, 3 additional wards were computerized [geriatrics, neurosurgery, revalidation]. A steering committee of CPOE, composed of various members (direction, doctors, pharmacists, nurses, data processing specialistsl is created. This committee allows the installation of the means necessary to the deployment of CPOE in the Institution. Structured teams for the deployment are created: medical and nurse coaches. From 2009 to 2012, the deployment of the software is carried out, covering 16 wards, the emergency room, the recovery room and the day-hospitals. CONCLUSION: The computerization of the drug supply chain is a challenge which concerns the institutional level. The assets of our hospital and our project were: - a strong management committee, making of this project a priority entering the strategical planning of the institution; - a steering committee allowing each type of actor to express his needs, and of prioriser requests; - a closer medical coaching; - teams of nurses coaches, accompanying each ward, during and after the deployment; - a dynamic IT team allowing a relay between the Institution and the data-processing company. These points appeared essential and are as many keys for a successful deployment.

Dental agenesis: genetic and clinical perspectives.

Dental agenesis is the most common developmental anomaly in humans and is frequently associated with several other oral abnormalities. Whereas the incidence of missing teeth may vary considerably depending on dentition, gender, and demographic or geographic profiles, distinct patterns of agenesis have been detected in the permanent dentition. These frequently involve the last teeth of a class to develop (I2, P2, M3) suggesting a possible link with evolutionary trends. Hypodontia can either occur as an isolated condition (non-syndromic hypodontia) involving one (80% of cases), a few (less than 10%) or many teeth (less than 1%), or can be associated with a systemic condition or syndrome (syndromic hypodontia), essentially reflecting the genetically and phenotypically heterogeneity of the condition. Based on our present knowledge of genes and transcription factors that are involved in tooth development, it is assumed that different phenotypic forms are caused by different genes involving different interacting molecular pathways, providing an explanation not only for the wide variety in agenesis patterns but also for associations of dental agenesis with other oral anomalies. At present, the list of genes involved in human non-syndromic hypodontia includes not only those encoding a signaling molecule (TGFA) and transcription factors (MSX1 and PAX9) that play critical roles during early craniofacial development, but also genes coding for a protein involved in canonical Wnt signaling (AXIN2), and a transmembrane receptor of fibroblast growth factors (FGFR1). Our objective was to review the current literature on the molecular mechanisms that are responsible for selective dental agenesis in humans and to present a detailed overview of syndromes with hypodontia and their causative genes. These new perspectives and future challenges in the field of identification of possible candidate genes involved in dental agenesis are discussed.

Abnormal dentin structure in two novel gene mutations [COL1A1, Arg134Cys] and [ADAMTS2, Trp795-to-ter] causing rare type I collagen disorders.

Histological and ultrastructural observations of dentin of two patients affected with rare types of type I collagen disorders are presented. In the first case, a homozygous nonsense mutation in ADAMTS2 (substitution of a codon for tryptophan by a stopcodon) causes type VIIC Ehlers-Danlos syndrome (EDS) with multiple tooth agenesis and focal dysplastic dentin defects. In the second case, a missense mutation in COL1A1 (substitution of arginine by cysteine) results in a type I EDS phenotype with clinically normal-appearing dentition. Tooth samples are investigated by using light microscopy (LM), transmission electron microscopy (TEM) and immunostaining for types I and III collagen, and tenascin. These are compared with samples from patients with types III and IV osteogenesis imperfecta (OI) in association with dentinogenesis imperfecta (DI), showing a consistently abnormal appearance of the dentin in all specimens, with variations being primarily those of degree of change. Similarities in histological changes include the alternating presence of normal and severe pathological areas in primary and secondary dentin, the latter being characterized by large canal-like structures in atubular areas. Ultrastructural evidence of pathological dentinogenesis include abnormal distribution, size and organization of collagen fibers, which may also be found in clinically unaffected teeth. The histological and ultrastructural changes seen can be explained on the basis of odontoblast dysfunction which may be secondary to the collagen defect, interfering with different levels of odontoblast cell function and intercellular communication. These observations on (ultra)structural dentin defects associated with the two novel gene mutations are the first ever reported.

Exercise and posture-related changes of atrial natriuretic factor and cardiac function in diabetes.

To study whether the release of atrial natriuretic factor (ANF) was altered in diabetic cardiac autonomic neuropathy (CAN), we determined plasma ANF concentrations during exercise and changes of posture in three groups of age- and sex-matched subjects (9 healthy subjects, 7 diabetic patients with CAN, and 7 diabetic patients without CAN). During exercise, plasma ANF concentrations rose threefold (P less than .001), and this increase was similar in the three groups. However, heart-rate response to exercise was impaired in the two groups of diabetic patients (P less than .004 vs. healthy subjects) but was more severely impaired in patients with CAN (P less than .03 vs. patients without CAN). In healthy subjects and patients without CAN, the increases of ANF during exercise correlated significantly with those of heart rate, systolic blood pressure, and rate-pressure product (P less than .01). In patients with CAN, the correlation was found exclusively with heart rate (P less than .01). An increase of ventricular ejection fraction occurred in all groups (P less than .001) but without showing statistical differences between groups. After 30 min of standing, a similar postural drop of plasma ANF concentrations (P less than .002) was observed in all subjects, reflecting preserved sympathetic control of vessels. In conclusion, exercise induces an increase of plasma ANF in diabetic patients with CAN. This increase, occurring similarly to healthy subjects, indicates that autonomic activation plays a minor role in ANF release during exercise. Impaired heart-rate response to exercise in patients without CAN suggests early damage of autonomic function, undetected by conventional rest tests.

Cerebral blood flow and perfusion reserve capacity in hemodynamic carotid transient ischemic attacks due to innominate artery stenosis.

Ischemia in the carotid artery territory due to atherosclerotic stenosis of the innominate artery is rare. We report a case in which transcranial Doppler ultrasonography (TCD) and SPECT with acetazolamide challenge proved the hemodynamic mechanism. The patient presented with three hypotensive TIAs in the right middle cerebral artery territory. Angiography showed a tight innominate artery stenosis and subclavian steal but no coexistent carotid or vertebrobasilar lesion. SPECT showed disturbed regional blood flow in the middle cerebral artery territory along with an exhausted perfusion reserve capacity. After angioplasty, flow velocities were normal and the perfusion reserve was restored. SPECT should be used to select patients at risk susceptible to benefit from angioplasty.

Validation of radionuclide cardiac output measurements during exercise.

A nongeometric radionuclide technique with correction for attenuation was used for the determination of cardiac output and stroke volume during exercise in nine normal subjects and in ten hypertensive patients. Simultaneous reference stroke volume (range 48-159 ml) and cardiac output (range 3.6-23.8 l/min) measurements were obtained by the Fick method. Data were collected at rest and during 60 degrees upright exercise, at two or three levels of increasing severity. Three statistical measurements were used for the comparison of both methods: correlation, precision, and accuracy. Radionuclide and Fick cardiac output measurements (n = 67, rest and exercise data) correlated well (r = 0.90). For stroke volume, the correlation was less (r = 0.64); however, the precision or random variability of both methods was similar for stroke volume (radionuclide: 8 ml or 9%; Fick: 16 ml or 16%). The accuracy or systematic error was defined as the mean difference between radionuclide and Fick measurements. The radionuclide method underestimated the Fick measurements. The systematic error was 18 +/- 18 ml for stroke volume and 2.4 +/- 2.4 l/m for cardiac output. A similar comparison of both methods was made on the absolute changes of stroke volume (r = 0.61; range -19 + 70 ml) and cardiac output (r = 0.82; range +1.6 + 16.4 l/m) between rest and exercise. The precision of the two methods was similar; the systematic error was 1.9 +/- 2.2 l/m for cardiac output and 6 +/- 17 ml for stroke volume. Thus, in these two groups of patients, although radionuclide and Fick cardiac output measurements at rest and during exercise correlated well, the radionuclide values were systematically and significantly lower.

Hemodynamic effects of felodipine at rest and during exercise in exertional angina pectoris.

To examine the antianginal effects of felodipine, a new calcium antagonist, 8 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 30 minutes after oral administration of 0.1 mg/kg of felodipine. Angina pectoris was always prevented after the drug was given and the exercise intensity was increased until recurrence of angina (5 patients) or exhaustion (3 patients). Hemodynamic data were also recorded at this higher exercise capacity. At rest and during submaximal exercise, felodipine increased heart rate and decreased arterial blood pressure and systemic vascular resistance. The prevention of angina pectoris was accompanied by lower mean pulmonary capillary wedge pressure, systemic vascular resistance and ST-segment depression; the pressure-rate product was unchanged. The 20% greater exercise capacity after felodipine was attended by a 20% increase in maximal cardiac output, a 17% increase in maximal heart rate and a 13% increase in maximal pressure-rate product; the maximal arterial blood pressure and ST-segment abnormalities were unchanged and the systemic vascular resistance was lower. The relation between ST-segment depression and the pressure-rate product during exercise was favorably influenced by felodipine. Thus, felodipine is an active antianginal drug; its major mechanism of action is to lower the systemic vascular resistance. The data also suggest that it improves coronary blood flow during exercise.

Effect of intracoronary thrombolytic therapy on exercise-induced ischemia after acute myocardial infarction.

Intracoronary streptokinase (SK) therapy increases vessel patency rate after acute myocardial infarction (AMI) and thus may lead to a greater exercise-induced myocardial ischemia. This hypothesis was tested in 39 patients enrolled in an angiographically randomized trial of intracoronary SK (19 treated with SK and 20 control subjects); all patients underwent thallium-201 scintigraphy at rest before acute angiography, as well as at rest and during stress 5 to 6 weeks after AMI. The patients were classified into 2 groups based on the presence (n = 13) or absence (n = 26) of complete obstruction of the infarct-related coronary artery at the end of the acute angiography. Semiquantitative score of myocardial thallium uptake was expressed as percent of maximal defect score. Thallium defect score at rest between admission and 5 to 6 weeks' study decreased from 10 +/- 16% units in the control group and from 23 +/- 14% units in the SK group (p = 0.01). This decrease was related to opening of the infarct-related artery (opening 23 +/- 16% vs occlusion 5 +/- 10%). The change in exercise-induced defect score was significantly (p = 0.01) larger in patients in the SK group (11 +/- 6% units) than in those in the control group (5 +/- 7% units). The perfusion defect during exercise was larger (p = 0.006) in patients with incomplete obstruction or reperfusion (10 +/- 6% units) than in patients with complete obstruction (3 +/- 7%). This difference was independent of the number of diseased coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary artery reperfusion in acute myocardial infarction: assessment by pre- and postintervention thallium-201 myocardial perfusion imaging.

In a randomized trial of intracoronary streptokinase (STK) therapy in acute myocardial infarction, 44 patients (21 control subjects and 23 patients treated with STK) underwent sequential thallium-201 planar imaging before angiography and after 4 hours (redistribution), 4 days and 6 weeks. Patients were classified according to the presence or absence of angiographic reperfusion of the infarct-related artery. The semiquantitative score of myocardial thallium uptake was expressed as percent of maximal defect score. Both in control and in STK-treated groups, thallium defect scores decreased over time, but this decrease was smaller in the control group (before angiography, 33 +/- 4%; redistribution, 29 +/- 4%; 4 days, 25 +/- 4%; and 6 weeks, 22 +/- 4%) than in the STK group (44 +/- 4%, 38 +/- 4%, 26 +/- 4% and 21 +/- 3%, respectively). In patients in whom reperfusion was achieved (20 STK-treated, 6 control subjects), a marked decrease in thallium score was observed (before angiography, 40 +/- 4%; redistribution, 32 +/- 4%; 4 days, 20 +/- 5%; and 6 weeks, 14 +/- 22%) compared with patients in whom reperfusion was not achieved (37 +/- 4%, 36 +/- 5%, 33 +/- 5% and 33 +/- 4%, respectively). These results indicate that serial thallium imaging is an accurate method of assessing changes in myocardial perfusion after acute myocardial infarction. Restoration of thallium uptake was observed after reperfusion of the infarct-related artery whether this recanalization was seen spontaneously or after successful thrombolysis.

Late recurrence of operated adrenocortical carcinoma: atrial natriuretic factor before and after treatment with mitotane.

A 62-year-old man arrived at our hospital with recurrence of Cushing's syndrome 14 years after successful surgery for adrenocortical carcinoma. Investigations demonstrated recurrence of a large tumor above the right adrenal area; it was found to be inoperable. The patient was treated initially with a new glucocorticoid antagonist, RU 486, and later with the adrenolytic agent mitotane (o,p'DDD). The latter achieved hypoadrenocorticism and a substantial reduction of tumor size. During the initial period, worsening hyperadrenocorticism resulted in a rise of atrial natriuretic factor and an inhibition of renin activity, consistent with an increase of cortisol and plasma volume. Changes in opposite direction were observed after treatment with mitotane.

Ejection fraction response to upright exercise in hypertension: relation to loading conditions and to contractility.

The respective roles of peripheral and myocardial determinants of exercise ventricular performance were studied in 10 normal volunteers and in 9 mildly hypertensive patients without evidence of coronary disease. Hemodynamic measurements and equilibrium blood pool scintigraphy were simultaneously performed at rest and during maximal upright exercise. In hypertensive patients, mean systolic and diastolic blood pressure were, respectively, 199 +/- 23 and 102 +/- 12 mm Hg at rest, and 271 +/- 28 and 113 +/- 8 mm Hg at peak exercise. Ejection fraction response to exercise was normal (increase by more than 5%) in 4 hypertensive patients (normal hypertensive group: 63 +/- 4 to 77 +/- 6%) and in volunteers (65 +/- 3 to 78 +/- 4%) and abnormal in 5 hypertensive patients (abnormal hypertensive group: 66 +/- 6 to 58 +/- 10% at peak exercise). The abnormal response in the abnormal hypertensive group was not due to an inadequate decrease in systemic vascular resistance during exercise. By contrast, the ratio systolic blood pressure/end-systolic volume, an index of contractility, decreased by 2.3 +/- 4.9 in the abnormal hypertensive group, whereas it increased by 9.8 +/- 9.1 in the normal hypertensive group and by 7.3 +/- 2 in volunteers. Thus, abnormal exercise ejection fraction response in mild hypertension was not related to increased afterload but rather to intrinsic myocardial factors.

HMPAO single-photon emission computed tomography in posterior circulation infarcts.

The sensitivity of single-photon emission computed tomography (SPECT) in evaluating posterior circulation infarcts compared with that of computed tomography (CT) or magnetic resonance imaging (MRI) remains unknown. In a hospital-based population, the authors studied SPECT, CT, and MRI in 35 consecutive patients presenting with acute infarction clinically localized in the thalamus (7), posterior cerebral artery (PCA) territory (15), brainstem (19), and cerebellum (3). Multiple infarcts were noted in 8 patients. Overall, the SPECT sensitivity was lower than that of MRI (21% vs 93%, p = 0.004) and CT (42% vs 65%, p = 0.046). The SPECT and CT sensitivities were not significantly different (67% vs 73%) for PCA infarcts. Performed within 24 hours, SPECT showed a relevant hypoperfusion in all PCA infarcts. For brainstem infarcts, CT (33%, p = 0.074) and MRI (91%, p = 0.004) were more sensitive than SPECT, which showed no hemispheric hypoperfusion. The sensitivity of the three imaging techniques was 100% for large cerebellar infarcts. For the small group of thalamic infarcts, the SPECT, CT, and MRI sensitivities were 14, 71, and 100%, respectively. Thus, SPECT compared to CT and MRI is not helpful in the subacute phase to localize PCA and cerebellar infarcts and is of limited value for thalamic infarcts. In the first hours, the absence of cerebral hypoperfusion in brainstem infarcts may help to differentiate them from hemispheric infarcts usually associated with profound hypoperfusion.

Is a lung perfusion scan obtained by using single photon emission computed tomography able to improve the radionuclide diagnosis of pulmonary embolism?

Planar pulmonary scintigraphy is still regularly performed for the evaluation of pulmonary embolism (PE). However, only about 50-80% of cases can be resolved by this approach. This study evaluates the ability of tomographic acquisition (single photon emission computed tomography, SPECT) of the perfusion scan to improve the radionuclide diagnosis of PE. One hundred and fourteen consecutive patients with a suspicion of PE underwent planar and SPECT lung perfusion scans as well as planar ventilation scans. The final diagnosis was obtained by using an algorithm, including D-dimer measurement, leg ultrasonography, a V/Q scan and chest spiral computed tomography, as well as the patient outcome. A planar perfusion scan was considered positive for PE in the presence of one or more wedge shaped defect, while SPECT was considered positive with one or more wedge shaped defect with sharp borders, three-plane visualization, whatever the photopenia. A definite diagnosis was achieved in 70 patients. After exclusion of four 'non-diagnostic' SPECT images, the prevalence of PE was 23% (n =15). Intraobserver and interobserver reproducibilities were 91%/94% and 79%/88% for planar/SPECT images, respectively. The sensitivities for PE diagnosis were similar for planar and SPECT perfusion scans (80%), whereas SPECT had a higher specificity (96% vs 78%; P =0.01). SPECT correctly classified 8/9 intermediate and 31/32 low probability V/Q scans as negative. It is concluded that lung perfusion SPECT is readily performed and reproducible. A negative study eliminates the need for a combined V/Q study and most of the 'non-diagnostic' V/Q probabilities can be solved with a perfusion image obtained by using tomography.

Oral manifestations of patients with Marfan syndrome: a case-control study.

OBJECTIVE: The purpose of this study was to conduct a complete analysis of the oral abnormalities of patients with Marfan syndrome. STUDY DESIGN: Twenty three patients with Marfan syndrome and 69 healthy controls were studied. The subjects were screened for cariologic and periodontal alterations, as well as structural defects of enamel and dentin. Data analysis was performed by using the t test, the chi-square test, and regression models. RESULTS: Patients aged 0 to 17 years were significantly at risk for caries. Local hypoplastic enamel spots were more frequent in Marfan syndrome and could be related to caries history of the deciduous dentition. Root deformity, abnormal pulp shape, and pulpal inclusions were a frequent finding in patients with Marfan syndrome. Calculus and gingival indices were significantly higher in the study group as well. CONCLUSIONS: This study shows the importance of early diagnosis of oral anomalies and timely treatment of dental problems in Marfan syndrome. A series of therapeutic guidelines to be integrated in treatment strategies is proposed.

Cranial suture biology and dental development: genetic and clinical perspectives.

Premature fusion of the calvarial bones at the sutures, or craniosynostosis (CS), is a relatively common birth defect (1:2000-3000) frequently associated with limb deformity. Patients with CS may present oral defects, such as cleft soft palate, hypodontia, hyperdontia, and delayed tooth eruption, but also unusual associations of major dental anomalies such as taurodontism, microdontia, multiple dens invaginatus, and dentin dysplasia. The list of genes that are involved in CS includes those coding for the different fibroblast growth factor receptors and a ligand of ephrin receptors, but also genes encoding transcription factors, such as MSX2 and TWIST. Most of these genes are equally involved in odontogenesis, providing a pausible explanation for clinical associations of CS with dental agenesis or tooth malformations. On the basis of the present knowledge on genes and transcription factors that are involved in craniofacial morphogenesis, and from dental clinics of CS syndromes, the molecular mechanisms that control suture formation and suture closure are expected to play key roles in patterning events and development of teeth. The purpose of this article is to review and merge the recent advances in the field of suture research at the genetic and cellular levels with those of tooth development, and to apply them to the dental clinics of CS syndromes. These new perspectives and future challenges in the field of both dental clinics and molecular genetics, more in particular the identification of possible candidate genes involved in both CS and dental defects, are discussed.