Since viable bacteria can persist in tooth cavities regardless of the technique used for caries removal, the objective of the present randomized clinical trial was to examine the microflora of primary teeth treated by complete or partial removal of carious dentin. Deciduous molars with acute carious lesions in the inner half of dentin and vital pulp were randomly divided into two groups of 16: complete removal, in which the carious dentin was completely removed with the help of a caries detector dye, and partial removal, in which the carious dentin was completely removed from the dentinoenamel junction and lateral walls, while the necrotic carious dentin from the cavity floor was only removed superficially. Dentin samples were obtained with a sterile No. 3 bur after caries removal and 3–6 months after protection with calcium hydroxide cement and restoration of the cavities with resin composite. The samples were stored in thioglycolate. Decimal dilutions were then prepared and seeded for the enumeration of Streptococcus spp., mutans streptococci, Lactobacillus spp. and total microorganisms. Before sealing, a larger number of microorganisms was detected in teeth submitted to partial caries removal compared to the complete removal group. However, after sealing the level of colonization was similar in the two groups for all microorganisms studied. The results suggest that persistence of bacteria does not seem to be a reason for reopening of cavities in deciduous teeth after partial caries removal.
Sincein vitroand animal studies suggest that the combination of starch with sucrose may be more cariogenic than sucrose alone, the study assessedin situthe effects of this association appliedin vitroon the acidogenicity, biochemical and microbiological composition of dental biofilm, as well as on enamel demineralization. During two phases of 14 d each, fifteen volunteers wore palatal appliances containing blocks of human deciduous enamel, which were extra-orally submitted to four groups of treatments: water (negative control, T1); 2 % starch (T2); 10 % sucrose (T3); and 2 % starch+10 % sucrose (T4). The solutions were dripped onto the blocks eight times per day. The biofilm formed on the blocks was analysed with regard to amylase activity, acidogenicity, and biochemical and microbiological composition. Demineralization was determined on enamel by cross-sectional microhardness. The greatest mineral loss was observed for the association starch+sucrose (P<0·05). Also, this association resulted in the highest lactobacillus count in the biofilm formed (P<0·05). In conclusion, the findings suggest that a small amount of added starch increases the cariogenic potential of sucrose.
Objective: To evaluate the association of the consumption of foods of the ultra-processed group (UPF) with inflammatory markers in the adolescent population in Northeastern Brazil.Design: A cross-sectional population-based study. Food consumption was evaluated using two 24-h dietary recalls using the NOVA classification for food processing levels. The following inflammatory markers were evaluated: adiponectin, IL-6, IL-8, C-reactive protein (CRP) and TNF-α. Multivariate linear regression was used to investigate the association between the percentage of UPF energy contribution and inflammatory markers.Setting: São Luís, Maranhão, Brazil.Participants: The sample consisted of 391 male and female adolescents, aged from 17 to 18 years.Results: The average daily energy consumption by adolescents was 8032·9 kJ/d, of which 26·1 % originated from UPF. The upper tertile (T3) of UPF consumption presented higher intake of simple carbohydrates, lipids, saturated fat, and Na and lower protein intake. Individuals in T3 presented higher serum leptin and CRP levels (P < 0·05). Adolescents with UPF energy consumption ≥30·0 % (tertile 3 of UPF) had a 79 % (exp (0·58) = 1·79) increase in IL-8 levels when compared with adolescents in tertile 1 of UPF (P = 0·013).Conclusions: The association between the consumption of UPF, poor quality diet and pro-inflammatory markers have important harmful effects that can be observed as early as in adolescence.
21 February 2017 in International Journal of Paediatric Dentistry
Chronic oral diseases are rarely studied together, especially with an emphasis on their common risk factors. This study examined the association of added sugar consumption on “chronic oral disease burden” among adolescents, with consideration of obesity and systemic inflammation pathways through structural equation modeling. A cross-sectional study was conducted of a complex random sample of adolescent students enrolled at public schools in São Luís, Brazil (n = 405). The outcome was chronic oral disease burden, a latent variable based on the presence of probing depth ≥4 mm, bleeding on probing, caries, and clinical consequences of untreated caries. The following hypotheses were tested: 1) caries and periodontal diseases among adolescents are correlated with each other; 2) added sugar consumption and obesity are associated with chronic oral disease burden; and 3) chronic oral disease burden is linked to systemic inflammation. Models were adjusted for socioeconomic status, added sugar consumption, oral hygiene behaviors, obesity, and serum levels of interleukin 6 (IL-6). All estimators of the latent variable chronic oral disease burden involved factor loadings ≥0.5 and P values <0.001, indicating good fit. Added sugar consumption (standardized coefficient [SC] = 0.212, P = 0.005), high IL-6 levels (SC = 0.130, P = 0.036), and low socioeconomic status (SC = −0.279, P = 0.001) were associated with increased chronic oral disease burden values. Obesity was associated with high IL-6 levels (SC = 0.232, P = 0.001). Visible plaque index was correlated with chronic oral disease burden (SC = 0.381, P < 0.001). Our finding that caries and periodontal diseases are associated with each other and with added sugar consumption, obesity, and systemic inflammation reinforces the guidance of the World Health Organization that any approach intended to prevent noncommunicable diseases should be directed toward common risk factors.