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Introduction The purpose of this study was to evaluate a protocol for systemic administration of rosiglitazone in mice in order to stimulate apoptosis of osteocytes in the jaws and to evaluate the effect of osteocyte apoptosis induced by rosiglitazone in the progression of periapical lesions in mice at 7, 21, and 42 days. Methods C57BL/6 mice at 4–5 weeks of age were used. In phase 1, mice ( n = 24) were treated with rosiglitazone (gavage, 10 mg/kg dose) or without (phosphate-buffered saline + 10% dimethyl sulfoxide) for 1, 2, or 3 weeks. We used the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and 4′-6-diamidino-2-phenylindole methods for quantification of apoptotic cells. In phase 2, mice ( n = 30) received rosiglitazone for 2 weeks or just vehicle for 1 week ( n = 30), and periapical lesions were induced for 7, 21, or 42 days. We performed the measurement of periapical lesions, tartrate-resistant acid phosphatase staining, dual-energy x-ray absorptiometry for the evaluation of bone mineral density (BMD) in long bone, and gene evaluation using real time quantitative polymerase chain reaction of osteocyte markers ( Sost , Hyou1 , and Dmp1 ) and receptor activator of nuclear factor kappa-B ligand (RANKL) ( Tnfsf11 ). Results It was observed that systemic administration of rosiglitazone for 2 weeks showed apoptosis of osteocytes in a more expressive manner. In phase 2, in the groups that received rosiglitazone, a trend toward larger periapical lesions was observed ( P > .05). Rosiglitazone also induced a greater number of osteoclasts and a greater expression of Sost and Hyou1 at 21 days of lesions. Moreover, there were no statistically significant differences in RANKL and Dmp1 expression or in the BMD of femurs. Conclusions Rosiglitazone stimulated apoptosis of osteocytes, interfering in the progression of periapical lesions in mice.

The antimicrobial peptides human β-defensins (hBDs) are encoded by β-defensin genes (DEFBs) and are possibly involved in caries susceptibility. In this study we aimed (1) to investigate the relationship between salivary hBDs and caries and (2) to evaluate the association of genetic polymorphisms in DEFB1 and microRNA202 (miRNA202) with salivary levels of hBDs and caries experience. Two data sets were available for this study, totalizing 678 Brazilian children. Dental examination and saliva collection were performed in all included children. The salivary level for hDB1, hBD2, and hBD4 was assessed by ELISA sandwich technique in 168 children. The DNA was extracted from saliva, and polymorphisms in DEFB1 and miRNA202 were analyzed by real-time PCR. Statistical analysis was performed to investigate the associations between caries experience, hBD salivary level, genotype, and allele distribution, with an alpha of 0.05. The hBD1 level was significantly higher in caries-free children (p < 0.0001). The miRNA202 was associated with a lower level of salivary hBD1 (p < 0.05). Also, the polymorphic distribution of miRNA202 was associated with caries (p = 0.006). The polymorphisms in DEFB1 were not associated with hBD salivary level and caries experience (p > 0.05). In conclusion, our results indicate that genetic polymorphism in miRNA202 is involved in hBD1 salivary level as well as caries experience in children.

Background. Polymer bur is a new technology that proposes to conserve the dentin that is capable of remineralization. Aim : To conduct a quantitative systematic review to evaluate the effect of polymer burs on the reduction of Streptococcus mutans and Lactobacillus after dentin carious excavation in deciduous teeth. Methods and Material: Two reviewers performed the database to identify the relevant clinical papers. Only papers in English that compared polymer burs with other caries removal techniques with the microbiological aspects as an outcome were included. Papers that evaluated only permanent teeth were excluded. Risk of bias was also assessed. Individual study effect sizes were calculated using Cohen’s d formula for the comparisons of microorganism reduction before and after carious excavation. Results: The search resulted in 12 non-duplicated papers. After the revision, only 2 were selected. The quantitative evaluation demonstrated that polymer bur reduces microorganism levels in carious dentin. The larger effect size observed was for Streptococcus mutans in the polymer bur technique (r=0.84; d=3.12), followed by Lactobacillus in the carbide bur technique (r=0.83; d=3.03). Conclusion: Polymer burs promoted a significant reduction of microorganism levels, mainly Streptococcus mutans in carious dentin .

Objective To evaluate and correlate, in the same research, the mRNA expression and the staining of RANK, RANKL, OPG, TLR2 and MyD88 by immunohistochemistry in the apical periodontitis (AP) progression in mice. Material and Methods AP was induced in the lower first molars of thirty-five C57BL/6 mice. They were assigned to four groups according to their euthanasia periods (G0, G7, G21 and G42). The jaws were removed and subjected to histotechnical processing, immunohistochemistry and real-time reverse transcription-PCR (qRT-PCR). Data were analyzed with parametric and nonparametric tests (α=0.05). Results An increase of positive immunoreactivity for RANK, RANKL, OPG, TLR2 and MyD88 was observed over time (p

O conhecimento dos eventos biológicos que ocorrem no periápice dos dentes com necrose pulpar se torna importante para compreender o desenvolvimento das lesões periapicais. Muitas são as moléculas e mediadores que participam na instalação da lesão periapical, a partir da infecção bacteriana que ocorre no interior dos canais radiculares. Assim, o objetivo do presente trabalho foi avaliar moléculas do sistema imune inato, da osteoclastogênese e metaloproteinases em lesões periapicais (LP) induzidas experimentalmente em camundongos knockout e wild type. Para esse objetivo, o presente estudo foi dividido em dois trabalhos distintos. O primeiro teve como objetivo avaliar a expressão de metaloproteinase 2 (MMP2) e metaloproteinase 9 (MMP9) durante a progressão da LP em camundongos knockout para TLR2 (TLR2 KO) e MyD88 (MyD88 KO), em comparação com camundongos wild type (WT). O segundo estudo avaliou a correlação da expressão gênica e imunomarcação de RANK, RANKL, OPG, TLR2 e MyD88 durante a progressão da LP em camundongos WT. No primeiro estudo lesões periapicais foram induzidas em molares inferiores de 54 camundongos TLR2 KO, MyD88 KO e WT (n=18/grupo). Após 7, 21 e 42 dias, os animais foram eutanaziados e as mandíbulas foram dissecadas e submetidas a processamento histotécnico. Os cortes histológicos foram submetidos a imunohistoquímica e posteriormente foi avaliada presença ou ausência de MMP2 e MMP9 nos diferentes grupos. No segundo estudo, 35 camundongos WT foram utilizados. As lesões periapicais foram induzidas nos primeiros molares inferiores de ambos os lados. Após 0 (G0), 7 (G7), 21 (G21) e 42 (G42) dias, os animais foram anestesiados e eutanasiados para que as mandíbulas fossem dissecadas e divididas ao meio.O lado direito das mandíbulas foi para o processamento histotécnico, para posterior marcação de RANK, RANKL, OPG, TLR2 e MyD88, por meio da imuno-histoquímica do lado esquerdo da mandíbula foi utilizado para a extração de RNA, para a determinação da expressão gênica de RANK (Tnfrsf11a), RANKL (Tnfrsf11), OPG (Tnfrsf11b), TLR2 (Tlr2) e MyD88 (Myd88) utilizando quantificação em Tempo Real da Reação da Polimerase em Cadeia (qRT-PCR). Para ambos os estudos, testes paramétricos e não paramétricos foram realizados com nível de significância de 5%. Foi possível observar, no primeiro estudo, que nos períodos iniciais da progressão da lesão periapical, houve um aumento na imunomarcação de MMP9 nos camundongos TLR2 KO e MyD88 KO, quando comparados aos WT, diferente da MMP2 que não se observou nenhum aumento na imunomarcação. No entanto, aos 42 dias observou-se uma redução da imunomarcação de MMP2 e um aumento da MMP9 nos camundongos TLR2 KO. Adicionalmente, no segundo estudo, foi possível observar um aumento da imunomarcação para RANK, RANKL, OPG, TLR2 e MyD88 durante a progressão da lesão periapical (p

The aim of this study was to evaluate the expression of MMP2 and MMP9 during apical periodontitis (AP) progression in TLR2 (TLR2 KO) and in MyD88 (MyD88 KO) knockout mice compared to wild type (WT) mice. AP was induced in mandibular first molars of TLR2 KO (n= 18), MyD88 KO (n= 18), and WT mice (n= 18). After 7, 21, and 42 days, the animals were euthanized and the jaws were dissected and subjected to histotechnical processing. Subsequent sections were stained by immunohistochemistry and evaluated for detection of MMP2 and MMP9. Statistical analysis of the semi-quantitative analysis of immunohistochemistry was performed using chi-square test (α = 0.05). In the initial periods of AP progression, an increased expression of MMP9 in the TLR2 KO and MyD88 KO mice was observed. In the final periods of AP progression, a reduction of MMP2 expression and an increase of MMP9 expression in the TLR2 KO mice were observed. MMP2 and MMP9 production was modulated for TLR2 and MyD88 during apical periodontitis progression. Resumo O objetivo deste estudo foi avaliar a expressão de MMP2 e MMP9 durante a progressão da periodontite apical (AP) em camundongos knockout para TLR2 (TLR2 KO) e MyD88 (MyD88 KO) comparados aos camundongos wild type (WT). A AP foi induzida nos primeiros molares inferiores dos camundongos TLR2 KO (n = 18), MyD88 KO (n = 18) e WT (n = 18). Após 7, 21 e 42 dias, os animais foram eutanaziados e as mandíbulas foram dissecadas e submetidas a processamento histotécnico. As lâminas foram coradas por imuno-histoquímica e analisadas para a detecção de MMP2 e MMP9. A análise estatística semi-quantitativa da imuno-histoquímica foi realizada pelo teste qui-quadrado (α = 0,05). Nos períodos iniciais de progressão AP, foi observada uma expressão aumentada de MMP9 nos camundongos TLR2 KO e MyD88 KO. Nos períodos finais de progressão AP, observou-se uma redução da expressão de MMP2 e um aumento da expressão de MMP9 nos camundongos TLR2 KO. A produção de MMP2 e MMP9 foi modulada por TLR2 e MyD88 durante a progressão da periodontite apical.

The purpose of this study was to evaluate the association between caries and body mass index (BMI) deviations in Brazilian schoolchildren and adolescents.A total of 237 three- to 15-year-old children, all undergoing treatment in a university pediatric dental clinic, was evaluated. Caretakers answered a questionnaire on sociodemographic, ethnicity, oral hygiene, and dietary information. The children's height was measured in centimeters, the weight in kilograms, and BMIs were calculated. A dental exam was done. All data were analyzed using Epi Info 7.1.5 and Graph Pad Prism 5.0 software with a significance level of five percent.The mean BMI in the studied population was 17.78 (±3.30 SD); all scores fell within the 12.5 to 30.0 BMI range. The distribution of decayed, missing, and filled primary and permanent teeth (dmft/DMFT) was statistically similar among normal weight, underweight, overweight, and obese children (P0.05). There was no correlation between BMI and caries experience. The univariate and multivariate analysis using modifier factors as covariables did not demonstrate an association between BMI status and caries experience (P0.05).BMI deviations are not associated with caries experience.

The present study aimed to evaluate qualitatively and quantitatively the products released by composites with different light sources when immersed in distilled water or artificial saliva. Thirty-six samples were obtained from the composites using a silicone matrix. Specimens were divided into 12 groups according to: Composite (Charisma®, FiltekTMSilorane or GC Kalore®), device used for the materials photoactivation (halogen light or LED) and immersion medium (distilled water orartificialsaliva). Measurements were obtained using a UV-visible spectrophotometer. The FiltekTMSilorane resin showed the highest absorbance and thus the highest concentration of monomers released at the maximum time assessed when immersed in artificial saliva. No significant difference was observed in the amount of monomers release when using LED (0.54 mg mL-1) and halogen light (0.53 mg mL-1). Release of monomers from composites can occur and is dependent on the composite formulation, immersion medium or the photoactivation unit.

Anterior open bite (AOB) has a multifactorial etiology caused by the interaction of sucking habits and genetic factors. The aim of this study was to evaluate the association between AOB and polymorphisms in genes that encode Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). Four hundred and seventy-two children that presented at least one sucking habit were evaluated. Children were examined clinically for the presence of AOB. Genomic DNA was extracted from saliva. Genotyping of the selected polymorphisms in MMP2, MMP3, MMP9, TIMP1 and TIMP2 was carried out by real-time PCR using the TaqMan method. Allele and genotype frequencies were compared between the groups with and without AOB using the PLINK® software in a free and in a recessive model using a chi-square test. Logistic regression analysis was implemented (p≤0.05). Two hundred nineteen children had AOB while 253 did not. The polymorphism rs17576 in MMP9 was significantly associated with AOB (p=0.009). In a recessive model GG genotype was a protective factor for AOB (p=0.014; OR 4.6, 95%CI 1.3-16.2). In the logistic regression analysis, none of the genes was associated with AOB. In conclusion, the polymorphism rs17576 (glutamine for arginine substitution) in MMP9 was a protective factor for AOB. Resumo A mordida aberta anterior apresenta uma etiologia multifatorial causada pela interação entre hábitos de sucção e fatores genéticos. O objetivo deste estudo foi avaliar a associação entre mordida aberta anterior e polimorfismo nos genes que codificam as metaloproteinases da matriz (MMPs) e seus inibidores teciduais (TIMPs). Foram avaliadas 472 crianças que apresentvam pelo menos um hábito de sucção. As crianças foram clinicamente examinadas para avaliar a presença de mordida aberta anterior. DNA genômico foi extraído da saliva. A genotipagem dos polimorfismos selecionados em MMP2, MMP3, MMP9, TIMP1 e TIMP2 foi realizada por PCR em tempo real, usando o método de TaqMan. As frequências alélicas e genotípicas foram comparadas entre os grupos com e sem mordida aberta anterior usando o software PLINK®. Duzentas e dezenove crianças apresentavam mordida aberta anterior enquanto 253 não a apresentavam. O polimorfismo rs17576 em MMP9 estava significativamente associado com mordida aberta anterior (p=0,009). No modelo recessivo (GG versus AG+AA) o genótipo GG foi um fator protetor para mordida aberta anterior (p=0,014; OR 4,6; 95%CI 1,3- 16,2). Concluindo, o polimorfismo rs17576 (substituição de glutamina por arginina) em MMP9 está associado com mordida aberta anterior. Os resultados obtidos suportam a hipótese de que fatores genéticos estão envolvidos com a etiologia da mordida aberta anterior.