In the last decade, several access cavity designs involveing minimal removal of tooth tissue have been described for gaining entry to pulp chambers during root canal treatment. The premise behind this concept assumes that maximum preservation of as much of the pulp chamber roof as possible during access preparation would maintain the fracture resistance of teeth following root canal treatment. However, the smaller the access cavity, the more difficult it may be to visualize and debride the pulp chamber as well as locate, shape, clean and fill the canals. At the same time, a small access cavity may increase the risk of iatrogenic complications as a result of poor visibility, which may have an impact on treatment outcome. This study aimed to critically analyse the literature on minimal access cavity preparations, propose new nomenclature based on self‐explanatory abbreviations and highlight the areas in which more research is required. The search was conducted without restrictions using specifics terms and descriptors in four databases. A complementary screening of the references within the selected studies, as well as a manual search in the highest impact journals in endodontics, namely International Endodontic Journal and Journal of Endodontics, was also performed. The initial search retrieved 1831 publications. The titles and abstracts of these papers were reviewed, and the full text of 94 studies was assessed. Finally, a total of 28 studies were identified as evaluating the influence of minimally invasive access cavity designs on the fracture resistance of teeth and on the different stages of root canal treatment (orifice location, canal shaping, canal cleaning, canal filling and retreatment). Overall, the studies had major methodological drawbacks and reported inadequate and/or inconclusive results on the utility of minimally invasive access preparations. Furthermore, they offered limited scientific evidence to support the use of minimally invasive access cavities to improve the outcome of root canal treatment and retreatment; they also provided little evidence that they preserved the fracture resistance of root filled teeth to a greater extent than traditional access cavity preparations. It was concluded that at present, there is a lack of supporting evidence for the introduction of minimally invasive access cavity preparation into routine clinical practice and/or training of undergraduate and postgraduate students.

Do orthodontic movements induce pulp necrosis? Weissheimer et al.

BackgroundControversial findings exist in the literature regarding the association between tobacco smoking and development of apical periodontitis or need for root canal treatment, with some studies reporting an increase in the prevalence of these outcomes in smokers, whilst others reporting no association.AimTo evaluate if there is scientific evidence to support an association between tobacco smoking and a greater prevalence of apical periodontitis and/or root canal treatments.Data SourcesA systematic search was performed using MeSH terms and free terms in the PubMed, Scopus, Virtual Health Library (VHL), Cochrane library and Open Gray databases.Study Eligibility Criteria, Participants and InterventionsObservational studies that evaluated the association between smoking and the development or healing of periapical lesion and/or the prevalence of root canal treatment in humans were included.Study Appraisal and Synthesis MethodsA quality assessment of included studies was performed, and the relevant information and findings were evaluated. A meta‐analysis using nine included studies was performed through RevMan software, and the certainty of evidence was evaluated through GRADE.ResultsFifteen studies were included, of which 10 were classified as low risk of bias, 4 were considered as moderate risk of bias and 1 as high risk of bias. Ten studies reported that smoking was associated with a greater prevalence of periapical periodontitis and/or root canal treatment. Five studies reported no association. Nine studies were included in the pooled meta‐analysis, comprising two subgroups: apical periodontitis and root canal treatment. From these nine studies, eight studies were included in the apical periodontitis subgroup meta‐analysis and demonstrated that this condition was significantly more prevalent in smokers when compared to the nonsmokers (odds ratio = 2.78[CI: 1.60, 4.85], P < 0.001; I2 = 79%; no adjusted odds ratio). Three studies were included in the root canal treatment subgroup meta‐analysis and demonstrated an increased prevalence in smokers when compared to the nonsmokers (odds ratio = 2.73 [CI: 1.06, 2.83], P < 0.001; I2 = 72%; no adjusted odds ratio). The pooled meta‐analysis demonstrated that smokers had twice the chance of having apical periodontitis and/or root canal treatment when compared to nonsmokers (odds ratio of 2.42 [CI: 1.59, 3.68], P < 0.01; I2 = 85%). The GRADE analysis demonstrated moderate certainty of evidence.LimitationsSeveral confounding factors were identified such as misinformation regarding the period of time subjects had smoked, as well as the frequency of smoking and the number of cigarettes consumed. No adjustment in odds ratio data for confounding was performed.Conclusions and Implications of Key FindingsThis systematic review and meta‐analysis indicate that tobacco smokers have an increased prevalence of periapical periodontitis and root canal treatments with moderate certainty of evidence.

Silva EJNL, Ferreira CM, Pinto KP, Barbosa AFA, Colac ßo MV, Sassone LM. Influence of variations in the environmental pH on the solubility and water sorption of a calcium silicate-based root canal sealer. International

AimTo evaluate the effects of alcohol and nicotine, when used alone or simultaneously, in the development of apical periodontitis induced in rats, using a correlative analytic approach with micro‐CT, histological and immunohistochemical analysis.MethodologyTwenty‐eight male Wistar rats were arranged into four groups: Control, Nicotine, Alcohol and Alcohol + Nicotine. The alcohol groups were exposed to self‐administration of a 25% alcohol solution, whilst the other groups drunk only filtered water. The nicotine groups received daily intraperitoneal injections of a solution with 0.19 μL of nicotine per mL, whilst the other groups received saline solution. The pulps of the left mandibular first molars were exposed for 28 days to induce periapical lesions. Throughout the experiment, drug administration was maintained, and the animals had their weight and solid and liquid consumption measured. After euthanasia, the mandibles were removed and the area, volume and major diameter of the periapical lesions were measured using micro‐computed tomography images. The samples were submitted to histopathological evaluation and immunohistochemistry for RANKL and PTHrP. Statistical analysis was undertaken with a significance level of 5%. Nonparametric data were analysed using the Kruskal–Wallis test followed by Dunn's test, whilst one‐way anova followed by Tukey's test was performed for parametric data.ResultsThe alcohol groups had lower solid and liquid consumption and gained less weight when compared to the nonalcohol groups (P < 0.05). The Alcohol + Nicotine group had lesions with significantly larger volume and area when compared to the other groups (P < 0.05), whilst the Alcohol or Nicotine groups had significantly larger lesions than the control group (P < 0.05). There was no significant difference in the largest diameter of the lesions amongst groups (P > 0.05). The experimental groups had greater inflammatory response scores than the control group (P < 0.05), and the representative samples had more pronounced immunoreaction against RANKL and PTHrP antibodies.ConclusionsAlcohol and nicotine consumption exacerbated the inflammatory response and the development of periradicular lesions in rats. The association of both substances enhanced their harmful effects.