Added Sugar Consumption and Chronic Oral Disease Burden among Adolescents in Brazil.

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.

Impact of resveratrol on bone repair in rats exposed to cigarette smoke inhalation: histomorphometric and bone-related gene expression analysis.

This study investigated the effect of resveratrol on bone healing and its influence on the gene expression of bone-related markers in rats exposed to cigarette smoke. Two calvarial defects were created in each of 60 rats, which were assigned equally (n=20) to three groups: (1) resveratrol (10mg/kg)+smoke exposure (SMK+RESV); (2) placebo+smoke exposure (SMK+PLA); or (3) placebo+no smoke exposure (NS+PLA). Substances were administered daily for 30days following surgery. Smoke inhalation was started 7days before surgery and continued for 30days after surgery. One defect was processed for histomorphometric analysis and the other was used for mRNA quantification of bone-related gene expression by qPCR. The remaining defect was smaller in the SMK+RESV (2.27±0.61mm, P=0.0003) and NS+PLA (2.17±0.74mm, P=0.0005) groups than in the SMK+PLA group (3.12±0.47mm). Higher levels of Runx2 were observed in the NS+PLA group than in the smoke exposure groups (vs. SMK+PLA, P=0002; vs. SMK+RESV, P=0.052); levels of Lrp-5 were also higher in the no smoke exposure group (vs. SMK+RESV, P=0.009; vs. SMK+PLA, P=0.003). Resveratrol therapy decreased RANKL/OPG expression when compared to placebo (SMK+RESV vs. SMK+PLA, P=0.017). Dkk1 levels were decreased in the SMK+RESV group when compared to the SMK+PLA (P=0.006) and NS+PLA groups (P=0.005). In conclusion, resveratrol optimizes the repair of critical-sized bone defects, up-regulating the gene expression of important bone remodelling markers in rats exposed to cigarette smoke inhalation.

Possible evidence of systemic lupus erythematosus and periodontal disease association mediated by Toll-like receptors 2 and 4.

Toll-like receptors (TLRs) participate in the innate immune response and trigger the immune responses of the body. Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown aetiology, characterized by an excessive autoimmune response in the body affecting the connective tissues. The disease is possibly triggered by both environmental aetiological factors and pathological organic processes such as exposure to sunlight, chronic infectious processes and genetic factors. Conversely, periodontal disease is an infectious disease caused by microorganisms in the oral cavity, resulting in a chronic inflammatory process which continuously stimulates the immune response, thus causing damage to the periodontal tissues. The expression of both TLR-2 and TLR-4 receptors are increased in both SLE and periodontal disease. Periodontitis might trigger excessive activation of immune response occurring in SLE by maintaining a high expression of TLRs, leading in turn to the acceleration of the onset and progression of autoimmune reactions. In addition, periodontal treatment is able to reduce the expression of these receptors and therefore the symptoms of SLE. Here we discuss the possible interaction between SLE and periodontitis, and suggest further studies evaluating common features in both factors that could explored, due to morbidity and mortality of SLE and the high incidence of periodontal infections around the world.

Possible involvement of IL-21 and IL-10 on salivary IgA levels in chronic periodontitis subjects.

Specific cytokines and the costimulatory protein CD40 play role in inducing immunoglobulin (Ig)A production by B cells in the humoral immune response. However, to date, the role of these mediators was not investigated in chronic periodontitis. Therefore, the aim of this study was to assess the local levels of interleukin (IL)-21, IL-21 receptor (IL-21R), IL-4, IL-10 and CD40 ligand (CD40L) on chronic periodontitis subjects and their relationship with the salivary levels of IgA. Gingival biopsies and un-stimulated saliva were collected from chronic periodontitis (n = 15) and periodontally healthy (n = 15) subjects. The mRNA levels of IL-4, IL-10, IL-21, IL-21R, CD40L in the gingival biopsies were evaluated by quantitative real-time polymerase chain reaction. The salivary levels of IgA and the levels of IL-4 and IL-10 in the gingival biopsies were analyzed by ELISA. The mean levels of IgA were significantly higher in the chronic periodontitis compared to periodontally healthy group (P < 0.05). The mRNA levels for IL-21 was higher (P < 0.05) in the chronic periodontitis when compared to the healthy group. However, the expression of IL-21R and CD40L did not differ between groups. The IL-10 was significantly elevated at mRNA and protein levels in chronic periodontitis when compared to periodontally healthy group (P < 0.05). Conversely, the mRNA levels as well as the protein amount of IL-4 were significantly lower (P < 0.05) in chronic periodontitis than healthy ones. In conclusion, the upregulation of IL-21 and IL-10 and downregulation of IL-4 in periodontitis tissues may be collectively involved in the increased levels of salivary IgA in chronic periodontitis subjects.

Morphological changes and EGF expression in the granular convoluted tubule cells of submandibular glands of Trypanosoma cruzi infected rats.

We have previously demonstrated in rats that Chagas' disease affects the salivary glands, by promoting an enlargement of the submandibular gland. In order to further investigate possible functional alterations on infected submandibular glands, the objective of the present study was to analyze epidermal growth factor (EGF) expression on rat submandibular glands during Trypanosoma cruzi infection. Results demonstrated that infected rats presented lower levels of testosterone, and morphological changes in the granular convoluted tubule (GCT) cells of the submandibular glands, along with acinar enlargement and delayed ductal maturation at the developing granular ducts. Immunohistochemistry analysis additionally showed that only few cells immunolabelled with anti-EGF on infected rats during the acute phase of Chagas' disease, while after 64 and 90 days (chronic phase) of infection, EGF expression was similar to non-infected rats. The present findings suggest that at the acute phase of Chagas' disease, lower levels of testosterone may lead to a delayed maturation of GCT, which positively correlates with decreased EGF production by submandibular glands cells.

Periodontal healing may be affected by aging: a histologic study in rats.

BACKGROUND AND OBJECTIVE: Although wound healing has been reported to be impaired with aging, very little is known about its effect on periodontal tissues. Therefore, the aim of this study was to evaluate, histologically in rats, the influence of aging on a spontaneous periodontal healing model. MATERIAL AND METHODS: Twenty-four male Wistar rats were used and assigned to the following groups: control (n = 12; 2 mo old) and aged (n = 12; 18 mo old). Fenestration defects (4 x 3 x 1 mm) were created bilaterally at the buccal aspect of the distal root of the first mandibular molars, and the mandibulae were retrieved 3 and 6 wk postoperatively. The percentage of bone fill and density of newly formed bone, new cementum formation (NC), and the extension of the remaining defect (ERD) were histometrically obtained. RESULTS: Intragroup analysis demonstrated that, except for cementum, all histological parameters significantly improved over time (p < 0.05). Intergroup analysis additionally showed that the defects were initially similar in size, and that at 3 wk aging negatively influenced newly formed bone (86.38 +/- 2.99% and 73.06 +/- 3.21%, p < 0.001, for groups control and aged, respectively), BF (75.84 +/- 16.53% and 57.70 +/- 22.28%, p = 0.014) and ERD (0.41 +/- 0.20 mm and 1.17 +/- 0.37 mm, p < 0.001). At 6 wk, aging negatively influenced newly formed bone (88.12 +/- 2.90% and 78.19 +/- 5.35%, p < 0.001, for groups control and aged, respectively) and ERD (0.01 +/- 0.006 mm and 0.34 +/- 0.18 mm, p = 0.003), but not BF (98.15 +/- 2.43% and 87.87 +/- 11.63%, p > 0.05). No new cementum was formed along the root surface in the above groups. CONCLUSION: Within the limits of the present study, data analysis suggests that aging may impair, but not prevent, periodontal healing.