Publications by authors named "Ann E Scott"

8 Publications

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Serum vitamin B12 is inversely associated with periodontal progression and risk of tooth loss: a prospective cohort study.

J Clin Periodontol 2016 Jan 18;43(1):2-9. Epub 2016 Jan 18.

Unit of Periodontology, University Medicine, Ernst-Moritz-Arndt University Greifswald, Greifswald, Germany.

Aim: The aim of this study was to investigate the association of serum vitamin B12 with the progression of periodontitis and risk of tooth loss in a prospective cohort study.

Materials And Methods: In the Study of Health in Pomerania, 1648 participants were followed from 2002-2006 to 2008-2012 (mean duration 5.9 years). Serum vitamin B12 was measured by chemiluminescent enzyme immunoassay. Probing pocket depth (PD) and clinical attachment loss (CAL) were measured to reflect periodontal status on a half-mouth basis at each survey cycle. Tooth numbers are based upon a full-mouth tooth count.

Results And Conclusions: In multivariate regression models, baseline vitamin B12 was inversely associated with changes in mean PD (Ptrend = 0.06) and mean CAL (Ptrend = 0.01), and risk ratios of tooth loss (TL; Ptrend = 0.006) over time. Compared to participants in the highest vitamin B12 quartile, those in the lowest quartile had 0.10 mm (95%CI: 0.03, 0.17; Pdifference = 0.007) greater increase in mean PD, 0.23 mm (95%CI: 0.09, 0.36; Pdifference = 0.001) greater increase in mean CAL and a relative risk of 1.57 (95%CI: 1.22, 2.03; Pdifference < 0.001) for TL. Stratified analyses showed stronger associations between vitamin B12 and changes in mean CAL among never smokers (Pinteraction = 0.058). Further studies are needed to understand the potential mechanisms of these findings.
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http://dx.doi.org/10.1111/jcpe.12483DOI Listing
January 2016

Serum α-Tocopherol Has a Nonlinear Inverse Association with Periodontitis among US Adults.

J Nutr 2015 May 11;145(5):893-9. Epub 2015 Feb 11.

Unilever Research and Development, Vlaardingen, The Netherlands;

Background: Previous experimental models suggest that vitamin E may ameliorate periodontitis. However, epidemiologic studies show inconsistent evidence in supporting this plausible association.

Objective: We investigated the association between serum α-tocopherol (αT) and γ-tocopherol (γT) and periodontitis in a large cross-sectional US population.

Methods: This study included 4708 participants in the 1999-2001 NHANES. Serum tocopherols were measured by HPLC and values were adjusted by total cholesterol (TC). Periodontal status was assessed by mean clinical attachment loss (CAL) and probing pocket depth (PPD). Total periodontitis (TPD) was defined as the sum of mild, moderate, and severe periodontitis. All measurements were performed by NHANES.

Results: Means ± SDs of serum αT:TC ratio from low to high quartiles were 4.0 ± 0.4, 4.8 ± 0.2, 5.7 ± 0.4, and 9.1 ± 2.7 μmol/mmol. In multivariate regression models, αT:TC quartiles were inversely associated with mean CAL (P-trend = 0.06), mean PPD (P-trend < 0.001), and TPD (P-trend < 0.001) overall. Adjusted mean differences (95% CIs) between the first and fourth quartile of αT:TC were 0.12 mm (0.03, 0.20; P-difference = 0.005) for mean CAL and 0.12 mm (0.06, 0.17; P-difference < 0.001) for mean PPD, whereas the corresponding OR for TPD was 1.65 (95% CI: 1.26, 2.16; P-difference = 0.001). In a dose-response analysis, a clear inverse association between αT:TC and mean CAL, mean PPD, and TPD was observed among participants with relatively low αT:TC. No differences were seen in participants with higher αT:TC ratios. Participants with γT:TC ratio in the interquartile range showed a significantly lower mean PPD than those in the highest quartile.

Conclusions: A nonlinear inverse association was observed between serum αT and severity of periodontitis, which was restricted to adults with normal but relatively low αT status. These findings warrant further confirmation in longitudinal or intervention studies.
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http://dx.doi.org/10.3945/jn.114.203703DOI Listing
May 2015

Feeding dysfunction in children with single ventricle following staged palliation.

J Pediatr 2014 Feb 22;164(2):243-6.e1. Epub 2013 Oct 22.

Division of Cardiology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI; Division of Adult Cardiovascular Medicine, Department of Internal Medicine, Medical College of Wisconsin, Milwaukee, WI.

Objective: To determine the prevalence of feeding dysfunction in children with single ventricle defects and identify associated risk factors.

Study Design: Patients aged 2-6 years with single ventricle physiology presenting for routine cardiology follow-up at the Children's Hospital of Wisconsin were prospectively identified. Parents of the patients completed 2 validated instruments for assessment of feeding dysfunction. Chart review was performed to retrospectively obtain demographic and diagnostic data.

Results: Instruments were completed for 56 patients; median age was 39 months. Overall, 28 (50%) patients had some form of feeding dysfunction. Compared with a normal reference population, patients with single ventricle had statistically significant differences in dysfunctional food manipulation (P < .001), mealtime aggression (P = .002), choking/gagging/vomiting (P < .001), resistance to eating (P < .001), and parental aversion to mealtime (P < .001). Weight and height for age z-scores were significantly lower in subjects with feeding dysfunction (-0.84 vs -0.33; P < .05 and -1.46 vs -0.56; P = .001, respectively). Multivariable analysis identified current gastrostomy tube use (P = .02) and a single parent household (P = .01) as risk factors for feeding dysfunction.

Conclusion: Feeding dysfunction is common in children with single ventricle defects, occurring in 50% of our cohort. Feeding dysfunction is associated with worse growth measures. Current gastrostomy tube use and a single parent household were identified as independent risk factors for feeding dysfunction.
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http://dx.doi.org/10.1016/j.jpeds.2013.09.030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3946833PMC
February 2014

William Gowers: the never completed third edition of the 'Bible of Neurology'.

Brain 2012 Oct 3;135(Pt 10):3178-88. Epub 2012 Sep 3.

Faculty of Health Sciences, University of Queensland, Brisbane 4027, Australia.

William Gowers' classic single-authored two-volume A manual of diseases of the nervous system appeared in a first edition in 1886 and 1888, and in a second edition in 1892 and 1893, with a third edition of Volume 1 in 1899. No third edition of Volume 2 ever appeared. However, in 1949 Critchley stated that he had seen part of a revision of this volume. Subsequent writers could not find this material, but it recently came to light at Gowers' old hospital at Queen Square, London. The present paper describes the rediscovered material, containing Gowers' handwritten alterations for a further edition of Volume 2, and substantial new material, at least in relation to nystagmus and myasthenia. Gowers' declining health, or a conflict between his planned new text and his contributions to the neurology segments (1899) of Allbutt's System of medicine, may explain why a third edition of Volume 2 of the Manual of diseases of the nervous system never appeared.
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http://dx.doi.org/10.1093/brain/aws181DOI Listing
October 2012

Ascorbate and α-tocopherol differentially modulate reactive oxygen species generation by neutrophils in response to FcγR and TLR agonists.

Innate Immun 2013 21;19(2):152-9. Epub 2012 Aug 21.

School of Dentistry and MRC Centre for Immune Regulation, University of Birmingham, St Chads Queensway, Birmingham, UK.

Periodontitis, a ubiquitous chronic inflammatory disease, is associated with reduced antioxidant defences and neutrophil hyperactivity in terms of reactive oxygen species (ROS) generation. Its phenotype is thus characterized by oxidative stress. We have determined the effect of antioxidant micronutrients ascorbate and α-tocopherol on neutrophil ROS generation. Peripheral neutrophils from periodontally-healthy individuals (n = 20) were challenged with phorbol myristate acetate, IgG-opsonised Staphylococcus aureus, Fusobacterium nucleatum or PBS in the presence and absence of micronutrients (50 µM). Total and extracellular ROS were measured by luminol and isoluminol chemiluminescence respectively. Total and extracellular unstimulated, baseline ROS generation was unaffected by α-tocopherol, but inhibited by ascorbate and a combination of both micronutrients. Fcγ-receptor (Fcγ-R)-stimulated total or extracellular ROS generation was not affected by the presence of individual micronutrients. However, the combination significantly reduced extracellular FcγR-stimulated ROS release. Neither micronutrient inhibited TLR-stimulated total ROS, but the combination caused inhibition. Ascorbate and the micronutrient combination, but not α-tocopherol, inhibited extracellular ROS release by TLR-stimulated cells. Such micronutrient effects in vivo could be beneficial in reducing collateral tissue damage in chronic inflammatory diseases, such as periodontitis, while retaining immune-mediated neutrophil function.
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http://dx.doi.org/10.1177/1753425912455207DOI Listing
September 2013

W R Gowers 1895: two unpublished post-graduate lectures.

Brain 2012 Oct 6;135(Pt 10):3165-77. Epub 2012 Mar 6.

The National Hospital for Neurology and Neurosurgery Queen Square London and the Reta Lila Weston Institute for Neurological Studies, University College London, UK.

On 10 May 1893, William Gowers began a series of weekly clinical demonstrations at the National Hospital for the Relief and Cure of the Paralysed and Epileptic at Queen Square, London. The contents of some of these demonstrations were published as 'Post-graduate Clinical Lectures' in the Clinical Journal, and in other learned periodicals. Some were also later included in his book Clinical Lectures on Diseases of the Nervous System. Recently, the manuscripts of what appear to be verbatim transcripts of two further but unpublished demonstrations from Gowers' course in 1895 came to light, one containing alterations made in Gowers' handwriting. The first concerned a case of disseminated sclerosis and its differentiation from hysterical paraplegia, the second transverse myelitis and its consequences for bladder function. Why these lectures were never published remains uncertain, but their relatively unedited contents reveal something of the neurological knowledge, diagnostic reasoning, clinical examination and teaching methods employed by one of the great pioneers of clinical neurology.
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http://dx.doi.org/10.1093/brain/aws029DOI Listing
October 2012

Mapping biological to clinical phenotypes during the development (21 days) and resolution (21 days) of experimental gingivitis.

J Clin Periodontol 2012 Feb 12;39(2):123-31. Epub 2011 Dec 12.

Unilever Oral Care, Bebington, UK.

Aim: To characterize and map temporal changes in the biological and clinical phenotype during a 21-day experimental gingivitis study.

Materials And Methods: Experimental gingivitis was induced over 21 days in healthy human volunteers (n = 56), after which normal brushing was resumed (resolution phase). Gingival and plaque indices were assessed. Gingival crevicular fluid was collected from four paired test and contra-lateral control sites in each volunteer during induction (Days 0, 7, 14 and 21) and resolution (Days 28 and 42) of experimental gingivitis. Fluid volumes were measured and a single analyte was quantified from each site-specific, 30s sample. Data were evaluated by analysis of repeated measurements and paired sample tests.

Results: Clinical indices and gingival crevicular fluid volumes at test sites increased from Day 0, peaking at Day 21 (test/control differences all p < 0.0001) and decreased back to control levels by Day 28. Levels of four inflammatory markers showed similar patterns, with significant differences between test and control apparent at Day 7 (substance P, cathepsin G, interleukin-1β, elastase: all p < 0.03) and peaking at Day 21 (all p < 0.002). Levels of α-1-antitrypsin showed no pattern.

Conclusions: Levels of substance P, cathepsin G, interleukin-1β and neutrophil elastase act as objective biomarkers of gingival inflammation induction and resolution that typically precede phenotypical changes.
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http://dx.doi.org/10.1111/j.1600-051X.2011.01825.xDOI Listing
February 2012

Proteomic analysis of a noninvasive human model of acute inflammation and its resolution: the twenty-one day gingivitis model.

J Proteome Res 2010 Sep;9(9):4732-44

Periodontal Research Group, School of Dentistry, College of Medical and Dental Sciences, University of Birmingham, St. Chads Queensway, Birmingham, B4 6NN, United Kingdom.

The 21-day experimental gingivitis model, an established noninvasive model of inflammation in response to increasing bacterial accumulation in humans, is designed to enable the study of both the induction and resolution of inflammation. Here, we have analyzed gingival crevicular fluid, an oral fluid comprising a serum transudate and tissue exudates, by LC-MS/MS using Fourier transform ion cyclotron resonance mass spectrometry and iTRAQ isobaric mass tags, to establish meta-proteomic profiles of inflammation-induced changes in proteins in healthy young volunteers. Across the course of experimentally induced gingivitis, we identified 16 bacterial and 186 human proteins. Although abundances of the bacterial proteins identified did not vary temporally, Fusobacterium outer membrane proteins were detected. Fusobacterium species have previously been associated with periodontal health or disease. The human proteins identified spanned a wide range of compartments (both extracellular and intracellular) and functions, including serum proteins, proteins displaying antibacterial properties, and proteins with functions associated with cellular transcription, DNA binding, the cytoskeleton, cell adhesion, and cilia. PolySNAP3 clustering software was used in a multilayered analytical approach. Clusters of proteins that associated with changes to the clinical parameters included neuronal and synapse associated proteins.
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http://dx.doi.org/10.1021/pr100446fDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950674PMC
September 2010