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

Human cytomegalovirus is present in odontogenic cysts

Introduction: Recent studies suggest that some viruses, including human cytomegalovirus (CMV), may be involved in the pathogenesis of periapical lesions. Since periapical cysts (PCs) represent the next stage in the evolution of periapical granuloma, it seemed reasonable to investigate the presence of CMV in PCs and any possible relationship between its presence and the clinical features of those cysts, as well as to compare the results obtained with corresponding findings in non-inflammatory lesions, like odontogenic keratocysts (OKCs). Methods: Samples of 33 PCs and 10 OKCs, obtained at the time of surgery, were used for the detection of CMV DNA by polymerase chain reaction. Presence of the virus was correlated with clinical and radiographic features of the cysts. Results: CMV was detected in 18 PCs (54.5%) and six OKCs (60%). The presence of CMV was more frequent in cyst samples collected from patients who reported previous episodes of acute infection. The presence of sinus tract was more frequent in CMV-positive cysts and CMV presence was less frequent in a group of cysts showing signs of acute inflammation at the time of sample collection. The mean sizes of CMV-positive and CMV-negative PCs were almost the same; CMV-positive OKCs were slightly larger than CMV-negative OKCs. None of these results proved to be statistically significant. Conclusion: The presence of CMV in the cystic wall is a common feature of both inflammatory and non-inflammatory odontogenic cysts. Although this study has not proved that CMV affects pathogenesis of odontogenic cysts, such a possibility could not be ruled out