In a cross‐sectional study design, we test the hypothesis whether childhood obesity is associated with reduced flow rate of stimulated whole saliva and dental caries. Obese adolescents (n = 65) with a mean age of 14.5 years and normal weight subjects (n = 65) with a mean age of 14.2 years were clinically examined with respect to dental caries, visible plaque accumulation (visible plaque index (VPI%)), gingival inflammation in terms of bleeding on probing (BOP%) as well as answered a questionnaire concerning medical history, medication, oral hygiene habits, smoking habits, and sociodemographic background. The flow rate of stimulated whole saliva (ml/min) was determined. BMI was calculated and adjusted for age and gender (BMI‐sds). The obese subjects exhibited higher number of decayed surfaces (DS), 0.7 vs. 0.1 (P = 0.008) and lower flow rate of stimulated whole saliva 1.2 vs. 2.0 ml/min (P < 0.001). Of obese patients, 17 subjects had VPI% >25 and 21 had BOP% >25, both compared to only 5 subjects of the normal weight with P values of 0.005 and <0.001, respectively. In a multivariate logistic regression model BMI‐sds was significantly associated with the flow rate of stimulated whole saliva less than the median value 1.5 ml/min (P < 0.001; odds ratio (OR) 1.36) as well as with DS (DS >0) (P = 0.002; OR 1.31) and the associations were not found to be confounded by any of the studied variables. The results indicate that childhood obesity is associated with reduced flow rate of stimulated whole saliva and dental caries and further strengthens obesity's negative effect on children's oral health.

The study demonstrates an association between obesity and periodontal risk indicators in adolescents that in the long term may lead to oral morbidity. This result further strengthens obesity's negative effect on teenagers' periodontal health and highlights the importance of a close collaboration between dentists and pediatricians in the prevention and treatment of obesity.

To test the hypothesis whether microbiota in oral biofilm is linked with obesity in adolescents we designed this cross‐sectional study. Obese adolescents (n = 29) with a mean age of 14.7 years and normal weight subjects (n = 58) matched by age and gender were examined with respect to visible plaque index (VPI%) and gingival inflammation (bleeding on probing (BOP%)). Stimulated saliva was collected. They answered a questionnaire concerning medical history, medication, oral hygiene habits, smoking habits, and sociodemographic background. Microbiological samples taken from the gingival crevice was analyzed by checkerboard DNA‐DNA hybridization technique. The sum of bacterial cells in subgingival biofilm was significantly associated with obesity (P < 0.001). The link between sum of bacterial cells and obesity was not confounded by any of the studied variables (chronic disease, medication, VPI%, BOP%, flow rate of whole saliva, or meal frequency). Totally 23 bacterial species were present in approximately threefold higher amounts, on average, in obese subjects compared with normal weight controls. Of the Proteobacteria phylum, Campylobacter rectus and Neisseria mucosa were present in sixfold higher amounts among obese subjects. The association between obesity and sum of bacterial cells in oral subgingival biofilm indicates a possible link between oral microbiota and obesity in adolescents.

BackgroundPatients with severe congenital neutropenia (SCN) often develop periodontitis despite standard medical and dental care. In light of previous findings that mutations in the neutrophil elastase gene, ELANE, are associated with more severe neutropenic phenotypes, we hypothesized an association between the genotype of SCN and development of periodontitis.MethodsFourteen Swedish patients with SCN or cyclic neutropenia harboring different genetic backgrounds were recruited for periodontal examination. Peripheral blood, gingival crevicular fluid (GCF), and subgingival bacterial samples were collected. The levels of cytokines and antibacterial peptides were determined in GCF and plasma by multiplex immunoassay and immunoblotting, respectively. Subgingival bacterial samples were analyzed using 16S rDNA pyrosequencing.ResultsELANE mutations correlated with more severe periodontal status than the HAX1 or unknown mutations in patients with SCN. The subjects with mutant ELANE had higher levels of IL-1β in GCF. Using principal coordinate analysis of the subgingival microbiota, patients with ELANE mutations and reference subjects with periodontitis tended to cluster differently from patients with HAX1 or unknown mutations and non-periodontitis reference subjects.ConclusionThis study demonstrates an association between ELANE mutations in SCN and the development of periodontitis with skewed subgingival microbiota, indicating a potential role of ELANE mutations in the pathogenesis of periodontitis.

The results of this study show that 40% of orally presented abstracts at IAPD congresses were followed by a subsequent scientific publication in a peer-reviewed journal.

The effect of the dentifrice ingredient triclosan (2,4,4'-trichloro-2'-hydroxyldiphenyl ether) on the production of interleukin (IL)-1beta and IL-6 was studied in human gingival fibroblasts challenged with tumor necrosis factor alpha (TNFalpha) in vitro. When gingival fibroblasts were treated simultaneously with triclosan (0.25, 0.5 microg/ml) and TNFalpha (10 ng/ml), the stimulatory effect of TNFalpha on IL-1beta production was reduced by the agent. In situ hybridisation showed that the TNFalpha-induced expression of IL-1beta mRNA was significantly reduced by triclosan. Furthermore, when the cells were treated simultaneously with a known protein kinase C (PKC) activator, phorbol 12-myristate-13-acetate (PMA) and TNFalpha in the presence of triclosan (0.5 microg/ml), the agent reduced the production of IL-1beta. In contrast to its effect on IL-1beta, triclosan did not influence the mRNA expression or the production of IL-6 induced by TNFalpha. The finding that triclosan reduces the production of the inflammatory mediator IL-1beta in gingival fibroblasts further supports the view that triclosan exhibits an anti-inflammatory effect.

No difference in caries experience or enamel defect was observed between the CsA and TAC group.

Gingival biopsies were taken from 13 renal transplant patients (mean age 26.5 yr), 11 of whom exhibited cyclosporin A (CsA)-induced gingival overgrowth. Control material was obtained from seven volunteers (mean age 28 yr). Gingival tissue components were analyzed by quantitative microscopy (stereology) on 5-microns-thick sections of interdental papillae. The volume density (Vv) of different tissue components and the surface density of epithelial ridges were calculated by conventional point and intersection counting. The study showed that the volume density of oral epithelium and the surface density of the epithelial ridges in the CsA-induced gingival overgrowth were significantly increased compared to normal gingival tissue. The connective tissue of the lesion exhibited a significant increase in volume density of cells, blood vessels and non-collagenous matrix with a corresponding decrease in the collagenous matrix. These results indicate that CsA-induced gingival overgrowth represents a tissue with an altered composition characterized by increased thickness of oral epithelium and relatively increased amount of cells, vessels, non-collagenous matrix and decreased collagenous matrix in the connective tissue.