Periodontitis and low cognitive performance: A population‐based study

alexandrossfakianakis shared this article with you from Inoreader Periodontitis and low cognitive performance: A population‐based study via Journal of Clinical Periodontology Abstract Aim To study the epidemiological association between periodontitis and low cognitive performance amongst older adults, within a representative sample of the US population. Materials and methods Data from 2086 older adults (≥60 years old), representative of 77.1 million people, were retrieved from the NHANES 2011–2014 database. Periodontitis cases were identified and classified according to the AAP/CDC criteria (mild, moderate, and severe). Cognitive function was assessed through the Consortium to Establish a Registry for Alzheimer's disease (CERAD), the Animal Fluency (AFT), the Digit Symbol Substitution (DSST) tests, and the global cognition score. The lowest non-survey weighted quartile for each cognitive test was defined as low cognitive performance. Simple and multiple regression analyses were performed. Results Moderate and severe periodontitis were significantly associated with a low DSST performance (OR = 1.66, and OR = 2.97, respectively). Each millimeter of increase in mean CAL was associated with a lower AFT (OR = 1.44), DSST (OR = 1.86), and global cognition (OR = 1.50) performance. Conclusions The findings of the present study suggest the presence of an independent association between periodontitis and low cognitive performance amongst older adults (≥60 years old). This article is protected by copyright. All rights reserved. View on Web

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Neuroinflammation related to the blood‐brain barrier and sphingosine‐1‐phosphate in a pre‐clinical model of periodontal diseases and depression in rats.

alexandrossfakianakis shared this article with you from Inoreader Neuroinflammation related to the blood‐brain barrier and sphingosine‐1‐phosphate in a pre‐clinical model of periodontal diseases and depression in rats. via Journal of Clinical Periodontology ABSTRACT Aim To explore the potential mechanisms of neuroinflammation (microglia, blood-brain barrier [BBB] permeability, and the sphingosine-1-phosphate [S1P] pathways) resulting from the association between periodontitis and depression in rats. Materials and methods This pre-clinical in vivo experimental study used Wistar rats, in which experimental periodontitis (P) was induced by using oral gavages with Porphyromonas gingivalis and Fusobacterium nucleatum. Then a chronic mild stress (CMS) model was implemented to induce depressive-like behavior, resulting in four groups: P with CMS (P+CMS+), P without CMS (P+CMS-), CMS without P (P-CMS+), and controls (P-CMS-). After harvesting brain samples, Protein/mRNA expression analyses and fluorescence immunohistochemistry were performed in the frontal cortex (FC). Results were analyzed by ANOVA tests. Results CMS exposure increased the number of microglia (an indicator of neuroinflammation) in the FC. In the combined model (P+CMS+), there was a decrease in the expression of tight junction proteins (zonula occludens-1 [ZO-1], occludin) and an increase in intercellular and vascular cell adhesion molecules (ICAM-1, VCAM-1) and matrix metalloproteinase 9 (MMP9), suggesting a more severe disruption of the BBB. The enzymes and receptors of S1P were also differentially regulated. Conclusions Microglia, BBB permeability, and S1P pathways could be relevant mechanisms explaining the association between periodontitis and depression. This article is protected by copyright. All rights reserved. View on Web

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Initial supplementary dose of dolutegravir in second-line antiretroviral therapy: a non-comparative, double-blind, randomised placebo-controlled trial

alexandrossfakianakis shared this article with you from Inoreader Initial supplementary dose of dolutegravir in second-line antiretroviral therapy: a non-comparative, double-blind, randomised placebo-controlled trial via Clinical Infectious Diseases Advance Access Abstract Background Dolutegravir concentrations are reduced by efavirenz induction effect necessitating twice daily dolutegravir dosing when co-administered. Efavirenz induction persists for several weeks after stopping, which could potentially select for dolutegravir resistance if switching occurred with unsuppressed HIV-1 RNA levels and standard dolutegravir dosing. We evaluated the need for a lead-in supplementary dolutegravir dose in adults failing first-line tenofov ir-emtricitabine-efavirenz (TEE). Methods We conducted a randomised, double-blind, placebo-controlled, phase 2 trial in Khayelitsha, South Africa. Eligible patients had virologic failure (two consecutive HIV-1 RNA≥1000 copies/mL) on first-line TEE. Participants were randomly assigned (1:1) to switch to tenofovir-lamivudine-dolutegravir (TLD) with a supplementary 50 mg dolutegravir dose or placebo taken 12 hours later for 14 days. Primary outcome was proportion with HIV-1 RNA<50 copies/mL at week 24. This study was not powered to compare arms. Results 130 participants were randomised (65 to each arm). Median baseline HIV-1 RNA was 4.0 log10 copies/mL and 76% had baseline resistance to both tenofovir and lamivudine. One participant died and two were lost to follow-up. At week 24, 55/64 (86%, 95% confidence interval [CI], 75–93%) in the supplementary dolutegravir arm and 53/65 (82%, 95% CI, 70–90%) in the placebo arm had HIV-1 RNA<50 copies/mL. Grade 3 or 4 adverse events were similar in frequency between arms. None of six participants (3 in each arm) eligible for resistance testing by 24 weeks developed dolutegravir resistance. Conclusions Our findings do not support the need for initial dolutegravir dose adjustment in patients switching to TLD who failed first-line TEE. View on Web

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