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Eileen Moritz,1,2,* Gabriele Jedlitschky,1,* Josefine Negnal,1 Mladen V Tzvetkov,1 Günter Daum,3,4 Marcus Dörr,2,5 Stephan B Felix,2,5 Henry Völzke,2,6 Matthias Nauck,2,7 Edzard Schwedhelm,4,8 Peter Meisel,9 Thomas Kocher,9 Bernhard H Rauch,1,2,10,* Birte Holtfreter9,* 1Institute of Pharmacology, Department of General Pharmacology, University Medicine Greifswald, Greifswald, Germany; 2German Center for Cardiovascular Research (DZHK), Partner Site Greifswald, Greifswald, Germany; 3Clinic and Polyclinic for Vascular Medicine, University Heart Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; 4German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Hamburg, Germany; 5Department of Internal Medicine B, University Medicine Greifswald, Greifswald, Germany; 6Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany; 7Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany; 8Institute of Clinical Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Humburg, Germany; 9Dental Clinics, Department of Periodontology, University Medicine Greifswald, Greifswald, Germany; 10Carl von Ossietzky Universität Oldenburg, Department of Human Medicine, Section of Pharmacology and Toxicology, Oldenburg, Germany*These authors contributed equally to this workCorrespondence: Bernhard H RauchCarl von Ossietzky Universität Oldenburg, Department of Human Medicine, Section of Pharmacology and Toxicology, Carl-von-Ossietzky-Str. 9-11, Oldenburg, 26129, GermanyTel +49 (0) 441 798 4930Fax +49 (0) 441 798 3088Email Bernhard.Rauch@uni-oldenburg.dePurpose: Periodontitis is an inflammatory disease of the oral cavity with an alarmingly high prevalence within the adult population. The signaling lipid sphingosine-1-phosphate (S1P) plays a crucial role in inflammatory and immunomodulatory responses. In addition to cardiovascular disease, sepsis and tumor entities, S1P has been recently identified as both mediator and biomarker in osteoporosis. We hypothesized that S1P may play a role in periodontitis as an inflammation-prone bone destructive disorder. The goal of our study was to evaluate associations between periodontitis and S1P serum concentrations in the Study of Health in Pomerania (SHIP)-Trend cohort. In addition, we investigated the expression of S1P metabolizing enzymes in inflamed gingival tissue.Patients and Methods: We analyzed data from 3371 participants (51.6% women) of the SHIP-Trend cohort. Periodontal parameters and baseline characteristics were assessed. Serum S1P was measured by liquid chromatography tandem mass spectrometry. The expression of S1P metabolizing enzymes was determined by immunofluorescence staining of human gingival tissue.Results: S1P serum concentrations were significantly increased in subjects with both moderate and severe periodontitis, assessed as probing depth and clinical attachment loss. In contrast, no significant association of S1P was seen with caries variables (number and percentage of decayed or filled surfaces). S1P concentrations significantly increased with increasing high-sensitivity C-reactive protein (hs-CRP) levels. Interestingly, inflamed compared to normal human gingival tissue exhibited elevated expression levels of the S1P-generating enzyme sphingosine kinase 1 (SphK1).Conclusion: We report an intriguingly significant association of various periodontal parameters with serum levels of the inflammatory lipid mediator S1P. Our data point towards a key role of S1P during periodontitis pathology. Modulation of local S1P levels or its signaling properties may represent a potential future therapeutic strategy to prevent or to retard periodontitis progression and possibly reduce periodontitis-related tooth loss.Keywords: sphingosine-1-phosphate, lipid mediator, periodontitis, inflammation

Objective: To explore associations between diabetes etiology (type 1 diabetes mellitus [T1DM] vs. T2DM) and glycemic control in the prediction of 5-year periodontal status change.Research Design and Methods: The Study of Health in Pomerania (SHIP) is a population-based stratified sample of German men and women. Healthy participants and those determined to have T2DM arose from the SHIP cohort, and T1DM participants were recruited from diabetes clinics in the catchment area that gave rise to SHIP. Dentate participants (n = 2,626; 53% women; 20-81 years of age) were included. Diabetes was determined via physician diagnosis and/or HbA(1c) ≥6.5% (uncontrolled diabetes >7.0%). Examiners blinded to diabetes status performed random half-mouth periodontal examinations, assessing probing depth (PD) and attachment loss (AL) (four sites/tooth) at baseline and follow-up. Participants were categorized into six groups as follows: 1) diabetes free (n = 2,280), 2) incident T2DM (n = 79), 3) controlled T2DM (n = 80), 4) uncontrolled T2DM (n = 72), 5) controlled T1DM (n = 43), and 6) uncontrolled T1DM (n = 72). In multivariable regressions, mean PD change (ΔMPD), mean AL change (ΔMAL), or incident tooth-loss values were regressed across the aforementioned diabetes categories.Results: Mean (SD) ΔMPD and ΔMAL values among all participants were -0.08 ± 0.5 mm and 0.08 ± 1.03 mm, respectively, and 34% lost one or more teeth. Relative to diabetes-free participants, those with uncontrolled T2DM experienced greater ΔMPD ± SE (P < 0.05), whereas participants with either uncontrolled T1DM or uncontrolled T2DM realized greater ΔMAL (P < 0.05). Uncontrolled T1DM and T2DM were both associated with an increased risk of future tooth loss (P < 0.05).Conclusions: Diabetes control, but not etiology, was associated with future tooth loss and accelerated AL progression. [ABSTRACT FROM AUTHOR]

Objective: Infection may be a type 2 diabetes risk factor. Periodontal disease is a chronic infection. We hypothesized that periodontal disease was related to A1C progression in diabetes-free participants.Research Design and Methods: The Study of Health in Pomerania (SHIP) is a population-based cohort in Germany including 2,973 diabetes-free participants (53% women; aged 20-81 years). Participants were categorized into four groups according to increasing baseline periodontal disease levels (percentage of sites per mouth with attachment loss >or=5 mm, determined a priori); sample sizes for each respective category were 1,122, 488, 463, and 479 (241 participants were edentulous). Mean absolute changes (year 5 minus baseline) in A1C (DeltaA1C) were regressed across periodontal categories while adjusting for confounders (e.g., age, sex, smoking, obesity, physical activity, and family history).Results: Across baseline periodontal disease categories, DeltaA1C +/- SEM values were 0.023 +/- 0.02, 0.023 +/- 0.02, 0.065 +/- 0.03, and 0.106 +/- 0.03 (P(trend) = 0.02), yielding an approximate fivefold increase in the absolute difference in DeltaA1C when dentate participants in the highest versus lowest periodontal disease category were compared; these results were markedly stronger among participants with high-sensitivity C-reactive protein >or=1.0 mg/l (P(interaction) = 0.01). When individuals who had neither baseline periodontal disease nor deterioration in periodontal status at 5 years were compared with individuals with both poor baseline periodontal health and longitudinal periodontal deterioration, mean DeltaA1C values were 0.005 vs. 0.143% (P = 0.003).Conclusions: Periodontal disease was associated with 5-year A1C progression, which was similar to that observed for a 2-SD increase in either waist-to-hip ratio or age in this population. [ABSTRACT FROM AUTHOR]

Staphylococcus aureus is one of the most common causes of hospital-acquired infections. At the same time, 25% of healthy persons are symptom-free S. aureus carriers, and they have an increased risk of developing nosocomial S. aureus septicemia. Paradoxically, their prognosis is much better than that of noncarriers. We compared the antibody profiles for carriers and noncarriers toward S. aureus superantigens. In carriers, we found high titers of neutralizing antibodies specific for those superantigens that are expressed by their colonizing strain. The results show that carriage status confers strain-specific humoral immunity, which may contribute to protection during S. aureus septicemia. Copyright © 2006 Infectious Diseases Society of America [ABSTRACT FROM AUTHOR]

OBJECTIVE: Oral leukoplakia is an oral lesion with a premalignant character. Besides smoking and alcohol, diabetes could be a risk factor. The aim is to search for such an association. RESEARCH DESIGN AND METHODS: Subjects with leukoplakia (N = 123) from the population-based Study of Health in Pomerania (SHIP) were matched 1:2 for age and sex with unaffected control subjects. Behavioral and lifestyle factors were assessed by a questionnaire. Lipoprotein concentrations, glycemia, and inflammation parameters were determined. RESULTS Subjects with oral leukoplakia showed higher levels of diabetes-related metabolites, a higher LDL/HDL cholesterol ratio (P = 0.004), and higher A1C (P = 0.002), and they were more frequently smokers (P < 0.001). Assessed by conditional logistic regression, the probability of leukoplakia increases with current smoking (odds ratio 2.20 [95% CI 1.16-4.17]) and higher levels of A1C (1.51 [95% CI 1.08-2.12]), revealing interaction between both factors (P = 0.012). CONCLUSIONS: Diabetes is associated with the risk of oral leukoplakia, which is exaggerated by smoking. The risk is positively correlated with A1C concentrations. [ABSTRACT FROM AUTHOR]