An exploratory study on the role of serum fatty acids in the short-term dietary therapy of gingivitis.

A previous randomised controlled trial showed that an anti-inflammatory diet (AID) significantly reduced gingival inflammation despite constant plaque values. This exploratory study investigated the role of serum fatty acids in relation to the observed clinical effects. Therefore, data of thirty participants with gingivitis, following either a pro-inflammatory dietary pattern (PID) rich in saturated fat, omega 6 fatty acids, and refined carbohydrates or an AID for 4 weeks, were correlated with corresponding serum samples for a variety of fatty acids. Changes in the fatty acid profile and effects on clinical periodontal parameters were analysed. Results showed that the polyunsatured:saturated fatty acids ratio (PUFA:SFA ratio) and nervonic acid level were significantly higher in the AID group than in the PID group at the end of the study. Significant intragroup differences were seen only in the AID group. Diverse fatty acids showed heterogeneous relations to clinical parameters. This study demonstrated that the serum fatty acid profile was not fundamentally associated with the clinical gingivitis-lowering effects of an AID in short-term, although some fatty acids showed individual relations to clinical parameters with respect to inflammation. Hence, short-term effects of dietary therapy on gingivitis may be rather based on carbohydrate-related effects and/or micronutrients

An oral health optimized diet can reduce gingival and periodontal inflammation in humans - a randomized controlled pilot study

BACKGROUND: The aim of this pilot study was to investigate the effects of four weeks of an oral health optimized diet on periodontal clinical parameters in a randomized controlled trial. METHODS: The experimental group (n = 10) had to change to a diet low in carbohydrates, rich in Omega-3 fatty acids, and rich in vitamins C and D, antioxidants and fiber for four weeks. Participants of the control group (n = 5) did not change their dietary behavior. Plaque index, gingival bleeding, probing depths, and bleeding upon probing were assessed by a dentist with a pressure-sensitive periodontal probe. Measurements were performed after one and two weeks without a dietary change (baseline), followed by a two week transitional period, and finally performed weekly for four weeks. RESULTS: Despite constant plaque values in both groups, all inflammatory parameters decreased in the experimental group to approximately half that of the baseline values (GI: 1.10 ± 0.51 to 0.54 ± 0.30; BOP: 53.57 to 24.17 %; PISA: 638 mm(2) to 284 mm(2)). This reduction was significantly different compared to that of the control group. CONCLUSION: A diet low in carbohydrates, rich in Omega-3 fatty acids, rich in vitamins C and D, and rich in fibers can significantly reduce gingival and periodontal inflammation. TRIAL REGISTRATION: German Clinical Trials Register; https://www.germanctr.de (DRKS00006301). Registered on 2015-02-21. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12903-016-0257-1) contains supplementary material, which is available to authorized users

Efficacy of Er:YAG laser on periodontitis as an adjunctive non‐surgical treatment: A split‐mouth randomized controlled study

Aim To evaluate the adjunctive efficacy of Er:YAG laser use with mechanical scaling and root planing (SRP ) for non‐surgical treatment of periodontitis. Materials and Methods In a randomized, single‐blinded, controlled trial, 27 patients were recruited. Using a split‐mouth design, two quadrants were randomly allocated into either a test group or a control group. The test quadrants received Er:YAG laser (ERL ; 100 mJ /pulse; 15 Hz to hard tissue and 50 mJ /pulse; 30 Hz to soft tissue) plus SRP treatment, while the control quadrants received SRP only. We evaluated periodontal indexes, including probing depth (PD ), clinical attachment level (CAL ), bleeding index (BI ), and plaque index (PLI ) at baseline, 3 months, and 6 months. Results The PD and CAL means in the ERL + SRP group were significantly lower than those in the SRP group at 3‐month follow‐up (PD : 2.98 ± 0.38 mm vs. 3.09 ± 0.35 mm; CAL : 4.51 ± 0.69 mm vs. 4.72 ± 0.67 mm) and 6‐month follow‐up (PD : 2.91 ± 0.31 mm vs. 3.02 ± 0.30 mm; CAL : 4.52 ± 0.65 mm vs. 4.72 ± 0.66 mm; p = 0.03 for both PD and CAL ). There were no significant differences in BI and PLI between two groups. Conclusions The Er:YAG laser treatment combined with conventional SRP significantly improved PD and CAL compared to SRP therapy alone; however, these differences were very small and, as a result, the adjunctive effect of Er:YAG laser is likely to be minimal clinically important

Retinoic acid reduces human neuroblastoma cell migration and invasiveness: effects on DCX, LIS1, neurofilaments-68 and vimentin expression

<p>Abstract</p> <p>Background</p> <p>Neuroblastoma is a severe pediatric tumor, histologically characterised by a variety of cellular phenotypes. One of the pharmacological approaches to neuroblastoma is the treatment with retinoic acid. The mechanism of action of retinoic acid is still unclear, and the development of resistance to this differentiating agent is a great therapy problem.</p> <p>Doublecortin, a microtubule-associated protein involved in neuronal migration, has recently been proposed as a molecular marker for the detection of minimal residual disease in human neuroblastoma. Nevertheless, no information is available on the expression of doublecortin in the different cell-types composing human neuroblastoma, its correlation with neuroblastoma cell motility and invasiveness, and the possible modulations exerted by retinoic acid treatment.</p> <p>Methods</p> <p>We analysed by immunofluorescence and by Western blot analysis the presence of doublecortin, lissencephaly-1 (another protein involved in neuronal migration) and of two intermediate filaments proteins, vimentin and neurofilament-68, in SK-N-SH human neuroblastoma cell line both in control conditions and under retinoic acid treatment. Migration and cell invasiveness studies were performed by wound scratch test and a modified microchemotaxis assay, respectively.</p> <p>Results</p> <p>Doublecortin is expressed in two cell subtypes considered to be the more aggressive and that show high migration capability and invasiveness.</p> <p>Vimentin expression is excluded by these cells, while lissencephaly-1 and neurofilaments-68 are immunodetected in all the cell subtypes of the SK-N-SH cell line. Treatment with retinoic acid reduces cell migration and invasiveness, down regulates doublecortin and lissencephaly-1 expression and up regulates neurofilament-68 expression. However, some cells that escape from retinoic acid action maintain migration capability and invasiveness and express doublecortin.</p> <p>Conclusion</p> <p>a) Doublecortin is expressed in human neuroblastoma cells that show high motility and invasiveness;</p> <p>b) Retinoic acid treatment reduces migration and invasiveness of the more aggressive cell components of SK-N-SH cells;</p> <p>c) The cells that after retinoic acid exposure show migration and invasive capability may be identified on the basis of doublecortin expression.</p

Testosterone, cortisol, and serotonin as key regulators of social aggression: A review and theoretical perspective

In human and non-human animals the steroid hormones cortisol and testosterone are involved in social aggression and recent studies suggest that these steroids might jointly regulate this behavior. It has been hypothesized that the imbalance between cortisol and testosterone levels is predictive for aggressive psychopathology, with high testosterone to cortisol ratio predisposing to a socially aggressive behavioral style. In this review, we focus on the effects of cortisol and testosterone on human social aggression, as well as on how they might modulate the aggression circuitry of the human brain. Recently, serotonin is hypothesized to differentiate between impulsive and instrumental aggression, and we will briefly review evidence on this hypothesis. The aim of this article is to provide a theoretical framework for the role of steroids and serotonin in impulsive social aggression in humans