Mineral trioxyde aggregate versus calcium hydroxide in apexification of non vital immature teeth: Study protocol for a randomized controlled trial

<p>Abstract</p> <p>Background</p> <p>Pulp necrosis is one of the main complications of dental trauma. When it happens on an immature tooth, pulp necrosis implies a lack of root maturation and apical closure. A therapy called apexification is required to induce the formation of a calcified apical barrier allowing a permanent and hermetic root filling. The aim of this prospective randomized clinical trial is to compare Mineral Trioxide Aggregate(MTA)with Calcium Hydroxide(CH)as materials used to induce root-end closure in necrotic permanent immature incisors.</p> <p>Methods/Design</p> <p>This study, promoted by AP-HP, was approved by the ethics committee(CPP Paris Ile de France IV). 34 children aged from 6 to 18 years and presenting a non-vital permanent incisor are selected. Prior to treatment, an appropriate written consent has to be obtained from both parents and from children. Patients are then randomly assigned to either the MTA(experimental)or CH(control)groups. Recalls are performed after 3, 6 and 12 months to determine the presence or absence of a calcified apical barrier through the use of clinical and radiographic exams. Additional criteria such as clinical symptoms, apical radiolucencies, periapical index(PAI)are also noted.</p> <p>Trial registration</p> <p>ClinicalTrials.gov no. <a href="http://www.clinicaltrials.gov/ct2/show/NCT00472173">NCT00472173</a> (First inclusion: May 10, 2007; Last inclusion: April 23, 2009; study completed: April 15, 2010)</p

Donner le sourire à nos jeunes patients : stratégies préventives et thérapeutiques

Les atteintes des structures dentaires ou les édentations peuvent perturber le développement psychique d’un enfant et les conséquences fonctionnelles engendrées peuvent s’exprimer à divers niveaux et degrés variables. Les traitements conservateurs et réhabilitations prothétiques permettent un développement physiologique et psychologique normal de l’enfant. Ces thérapeutiques rendent le sourire et une apparence normale grâce à des reconstitutions esthétiques, à la compensation de dents antérieures absentes et au maintien de la dimension verticale. Elles rétablissent les fonctions perturbées et préviennent leurs conséquences néfastes, assurant ainsi une croissance harmonieuse. La dimension esthétique revêt une importance capitale dans ces traitements mais ne doit pas se faire au détriment de la pérennité de la restauration. Le maintien d’organes dentaires en bonne santé demeure le meilleur garant du sourire de nos jeunes patients

Conséquences bucco-dentaires d'une naissance prématurée

MONTROUGE-BUFR Odontol.PARIS5 (920492101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Prise en charge bucco-dentaire d’une jeune patiente atteinte d’hypoplasie dermique en aires de Goltz

L’hypoplasie dermique en aires de Goltz est un syndrome génétique polydysplasique affectant les tissus d’origines ectodermique et mésodermique. Parmi l’ensemble des signes cliniques, les troubles bucco-dentaires occupent une place importante. La prise en charge thérapeutique de ces patients est complexe tant les affections dentaires et parodontales sont variées dans leur forme et leur sévérité. Nous présentons ici le cas d’une jeune patiente suivie dans le service d’odontologie de l’Hôpital Bretonneau

Reduction of stress-induced analgesia but not of exogenous opioid effects in mice lacking CB1 receptors

CB1 cannabinoid receptors are widely distributed in the central nervous system where they mediate most of the cannabinoid-induced responses. Here we have evaluated the interactions between the CB1 cannabinoid receptors and the endogenous opioid system by assaying a number of well-characterized opioid responses, e.g. antinociception and stress-mediated effects, on mutant mice in which the CB1 receptor gene was invalidated. The spontaneous responses to various nociceptive stimuli (thermal, mechanical and visceral pain) were not changed in mutant CB1 mice. Furthermore, the absence of the CB1 cannabinoid receptor did not modify the antinociceptive effects induced by different opioid agonists: morphine (preferential mu opioid agonist), D-Pen2-D-Pen5-enkephalin (DPDPE) and deltorphin II (selective delta opioid agonists), and U-50,488H (selective kappa opioid agonist) in the hot-plate and tail-immersion tests. In contrast, the stress-induced opioid mediated responses were modified in CB1 mutants. Indeed, these mutants did not exhibit antinociception following a forced swim in water at 34 degrees C and presented a decrease in the immobility induced by the previous exposure to electric footshock. However, the antinociception induced by a forced swim in water at 10 degrees C was preserved in CB1 mutants. These results indicate that CB1 receptors are not involved in the antinociceptive responses to exogenous opioids, but that a physiological interaction between the opioid and cannabinoid systems is necessary to allow the development of opioid-mediated responses to stress.Journal ArticleResearch Support, Non-U.S. Gov'tFLWINinfo:eu-repo/semantics/publishe

Inhibition of Both Angiotensin-Converting Enzyme and Neutral Endopeptidase by S21402 (RB105) in Rats With Experimental Myocardial Infarction

The vasoconstrictor angiotensin II and atrial natriuretic peptide (ANP) are oppositely involved in the development of heart failure, as modeled by myocardial infarction (MI) in rats. MI is a model also characterized by sodium retention despite the elevated plasma ANP levels, showing a desensitization of responses to ANP. S21402 (RB105) {N-[2S,3R-(2- mercaptomethyl-1-oxo-3-phenylbutyl) L-alanine]} is a dual inhibitor that inhibits both neutral endopeptidase (K(i) = 1.7 ± 0.3 nM) and angiotensin- converting enzyme (K(i) = 4.2 ± 0.5 nM). Inhibition of neutral endopeptidase protects endogenous ANP, and inhibition of angiotensin-converting enzyme blocks angiotensin II production, whereas inhibition of both peptidases is required to protect endogenous bradykinin (BK). Induction of MI in rats, by ligation of the left coronary artery, increased the base-line plasma ANP, cyclic GMP (cGMP) and renin concentrations, which were related to the degree of MI (moderate and severe MI rats). Urinary excretion of ANP. cGMP and BK was also increased in MI rats and was linked to the infarction size. S21402 (RB105) (25 mg/kg bolus plus 25 mg/kg/hr i.v.) decreased the mean blood pressure and increased natriuresis in MI rats whatever the degree of MI. S21402 (RB105) induced an increase in plasma renin in MI rats despite the elevated base-line levels. S21402 (RB105) did not alter the plasma ANP in MI rats. However, plasma cGMP was increased by the dual inhibitor, as a function of the infarction severity. Urinary excretion of ANP, cGMP and BK was also increased by S21402 (RB105), proportionally to the infarction size. Whatever the degree of MI, S21402 (RB105) was able to induce natriuresis, characterized by a desensitization of ANP-induced renal responses. Inhibition of both angiotensin-converting enzyme and neutral endopeptidase by potentiating endogenous ANP and BK and blocking angiotensin II production could be an interesting therapeutic approach in heart failure