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Bezerra da Silva RA, Nelson-Filho P, Lucisano MP, De Rossi A, de Queiroz AM, Bezerra da Silva LA. Aim To characterize the formation and progression of experimentally induced periapical lesions in teeth of MyD88 knockout (MyD88 KO) mice compared with wild-type (WT) mice. Methodology Periapical lesions were induced in the mandibular first molars of 30 WT and 30 MyD88 KO mice. After 7, 21 and 42 days, the animals were euthanized and the mandibles were subjected to histotechnical processing. Histological sections were stained with haematoxylin and eosin (HE), TRAP histoenzymology, Brown and Brenn staining and immunohistochemistry (RANK, RANKL, OPG). Data were subjected to statistical analysis by the nonparametric Mann-Whitney and Kruskal-Wallis tests and the Dunn post-test, using the SPSS software, version 17.0 (a = 0.05). Results Regarding the periapical lesion size, the MyD88 KO group had significantly higher values than the WT group in the periods of 7 (P = 0.001) and 21 days (P = 0.05). A larger number of neutrophils in the MyD88 KO group were observed (P = 0.01 at 7 days, P = 0.004 at 21 days and P < 0.001 at 42 days). Regarding the number of osteoclasts, no statistically significant difference was observed between the groups at any of the experimental periods (P = 0.884 at 7 days, P = 0.506 at 21 days and P = 0.211 at 42 days). Conclusions In the absence of MyD88, the animals had larger periapical lesions, with a severe inflammatory infiltrate and a significantly larger number of neutrophils.

Two-session root canal treatment using a calcium hydroxide-based dressing was associated with significantly smaller periapical lesions at 90 days and characterized by progressive repair.

To evaluate one-session endodontic treatment with aPDT and two-session treatment with calcium hydroxide (CH)-based dressing in dog's teeth with apical periodontitis. After experimental induction of apical periodontitis, 48 teeth were randomly assigned to the following groups: groups OS/aPDT120d and OS/aPDT180d (one-session treatment with aPDT) and groups TS/CH120d and TS/CH180d (two-session treatment with CH-based dressing-control groups). The animals were euthanized after 120 and 180 days. After histotechnical processing, microscopic and radiographic analyses were performed. Data were analyzed by Kruskal-Wallis and Fisher's exact tests (α = 0.05). Groups TS/CHs presented repaired resorbed cemental areas, with collagen bundles and few inflammatory cells. In groups OS/aPDTs, the areas of cemental resorption were not repaired with reduced presence of cells and fibers. In the analysis of the apical closure, fluorescence microscopy and percentage of radiographic reduction of lesions, there was significant difference between groups TS/CH120d and OS/aPDT120d and between TS/CH180d and OS/aPDT180d (p < 0.05). Groups TS/CHs had weak RANKL expression and positive immunostaining for RANK and OPG. In OS/aPDT120d, there was positive immunostaining for RANKL. In OS/aPDT180d, the three osteoclastogenesis markers were expressed. The results using aPDT were worse than those obtained with two-session endodontic treatment using a CH-based dressing in teeth with apical periodontitis.

Objectives To evaluate the microbial contamination of pacifiers by Mutans Streptococci (MS) and the efficacy of different methods for their disinfection.Methods Twenty-eight children were assigned to a 4-stage changeover system with a 1-week interval. In each stage, children received a new pacifier and the parents were instructed to maintain their normal habits for 1 week. After this time, the pacifiers were subjected to the following 4 disinfection methods: spraying with 0.12% chlorhexidine solution, Brushtox® or sterile tap water, and immersion in boiling tap water for 15 minutes. Microbiological culture for MS and Scanning Electron Microscopy (SEM) were performed. The results were analyzed statistically by Friedman’s non-parametric test (a=0.05).Results The 0.12% chlorhexidine spray was statistically similar to the boiling water (p>0.05) and more effective than the Brushtox® spray and control (p<0.05). The analysis of SEM showed the formation of a cariogenic biofilm in all groups with positive culture.Conclusions Pacifiers become contaminated by MS after their use by children and should be disinfected routinely. Spraying with a 0.12% chlorhexidine solution and immersion in boiling water promoted better disinfection of the pacifiers compared with a commercial antiseptic toothbrush cleanser (Brushtox®).

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Aim To evaluate the effect of alendronate (ALN) on the development of periapical lesions induced in ovariectomized rats. Methodology Twenty‐five rats were divided into three groups: sham (control), ovariectomy (OVX) and OVX + ALN. One day after OVX, animals from the OVX + ALN group received the medication via gavage. After 9 weeks, the first molars of all animals were submitted to periapical lesion induction. After 21 days, the animals were euthanized. Femurs were analysed for bone mineral density. The blocks of bone tissue containing the mandibular first molars were submitted to histotechnical processing and staining with haematoxylin and eosin (HE) for periapical lesion analysis under conventional microscopy. At the same time, the morphometric analysis of the periapical lesion area was performed in the fluorescence mode, as well as the histoenzimology for the quantification of osteoclasts and 4′‐6‐diamidino‐2‐phenylindole staining for the quantification of apoptotic osteocytes. In addition, the first maxillary molars were used for analysis of the gene expression of proinflammatory cytokines (IL‐1β, IL‐6 and TNF‐α) and osteoclastogenesis markers (RANKL/OPG). The results were submitted to ANOVA and Kruskal–Wallis tests and Tukey and Dunn post‐tests (significance level of 5%). Results Ovariectomy reduced bone mineral density of the femur, and treatment with ALN was able to prevent bone loss (P < 0.001). Regarding the microscopic analysis of the periapical region, the sham and OVX + ALN groups had moderately increased periodontal ligament and inflammatory infiltrate, while the OVX group had these parameters increased intensely. The periapical lesions of the OVX group were significantly larger in area in comparison to the other groups (P < 0.001). The OVX group had the largest amount of apoptotic osteocytes, and ALN was able to prevent the apoptosis of these cells, in addition to significantly reducing IL‐6 expression (P < 0.05). OVX and ALN had no effect on RANKL/OPG expression and did not influence the number of osteoclasts around the periapical lesion (P > 0.05). Conclusion The hypoestrogenic condition induced by OVX aggravated bone resorption, inducing the death of osteocytes and provoking larger periapical lesions. ALN treatment inhibited osteocyte apoptosis and inflammation via IL‐6, inhibiting bone resorption in periapical lesions of ovariectomized rats.

International Journal of Paediatric Dentistry 2014; 24: 367-372Background. Toothbrushes harbor a high number of cariogenic microorganisms. Aim. To investigate the viability of mutans streptococci (MS) on toothbrushes bristles and the production of extracellular polysaccharide (ECP) related to drying time. Design. Twenty children were submitted to brushing without dentifrice. Toothbrushes were kept at room temperature from 0 to 48 h and then submitted to microbiological processing. The number of MS colonies/biofilms was expressed according to scores: 0 = no colonies were detected; 1 = 1 to 50; 2 = 51 to 100; 3 = over 100. The amount of ECP was evaluated according to scores: 0 = absence; 1 = ECP recovering until 50% of the surface; 2 = ECP recovering more than 50% of the surface. Data were analyzed by Wilcoxon test (a = 5%). Results. At the periods of 0 to 16 h, the toothbrushes had intense bacterial contamination (score 3). From the 18-h, there was a statistically significant decrease in the MS viability (P = 0.0078), with predominance of score 1 on periods of 20 to 44 h. The most detected ECP amount was at 0-and 12-h period (P < 0.05) with reduction until 32-h period. Conclusions. Mutans streptococci remained viable on toothbrushes bristles, in vivo, for 44 h.