Summary
Objectives
The aim of this prospective, clinical single-centre study was to evaluate the masking efficacy of post-orthodontic resin infiltration after 12-month follow-up and correlate ...quantitative and qualitative outcome measures.
Methods
Patients with completed fixed orthodontic treatment and the presence of one or more vestibular active non-cavitated white spot lesion/s (WSL) ICDAS 1 or 2 (International Caries Detection and Assessment System) were provided with resin infiltration 3–12 months after bracket removal. All patients (n = 31) participating before (t0) intervention were invited again and examined after 12 months (t2). Enamel demineralization was scored using quantitative light-induced fluorescence QLF (DeltaFflourescence, DeltaQlesion volume, White Spot Area) and qualitative visual rating 11-point Likert-scale from 0 (no lesions visible on any tooth) to 10 (all teeth affected on the entire vestibular surface).
Results
In 17 patients (7 female and 10 male) 112 WSL (ICDAS 1: n = 1; ICDAS 2: n = 111) in 112 teeth were (re)examined. Before treatment (t0) a significant, weak (DeltaF), and moderate (DeltaQ, White Spot Area) correlation was observed between the quantitative and the qualitative rating (P < 0.002) median DeltaF: −7.31 (−10.4/−6.58)%; DeltaQ:−2.25 (−10.8/−0.41)% mm2; White Spot Area: 0.34 (0.05/1.16) mm2; visual rating:3.7 ± 1.2. Resin infiltration led to significantly increased fluorescence and decreased visual scores (P < 0.001) 7 days (t1) and 12 months (t2) after treatment. No significant changes based on DeltaF −6.55 (−7.29/−6.08)% and on visual ratings 1.0 ± 1.0 were observed between t1 and t2 (P = 1.000). After 7 days (t1) the correlation between the quantitative and the qualitative ratings remained significant, weak to moderate (P < 0.002). After 12 months (t2) the correlation was (non-)significant and weak for DeltaF, DeltaQ, and White Spot Area (P ≤ 0.097).
Limitations
Since the overall masking efficacy of resin infiltration has been shown previously, an untreated control group was omitted.
Conclusions
When assessing the masking efficacy of infiltrated post-orthodontic WSL only a weak to moderate correlation was found between QLF values and visual ratings. Furthermore, over time this correlation decreased. Thus, it remains unclear if QLF is a viable method to assess and quantify infiltrated post-orthodontic WSL over time.
Trial registration
German Clinical Trials Register (DRKS-ID:DRKS00005067).
Previous work has shown qualitatively that detection of demineralized tooth areas (white spot lesions, WSLs) is more reliable in digital photographs (DP) as in quantitative light-induced fluorescence ...(QLF) images. Based on non-rigid, multimodal image registration, we now quantitatively compare manual and automatic markings in both modalities.
After braces removal, pairs of DP and QLF were acquired from 124 teeth of 31 patients. Three experienced raters marked the WSL on both DP and QLF images, each of which was presented twice in randomized order. For each tooth and each modality, a ground truth (GT) was established using the simultaneous truth and performance level estimation algorithm on the total of six manual markings per image. DP and QLF image pairs were spatially registered, by aligning the outline of the tooth area in DPs to that of the corresponding tooth area in QLF. Between all pairs of markings for all teeth, position and size were compared quantitatively by the Dice coefficient and the novel coefficient of inclusion.
Our hypotheses: (i) the clinical inspection supported by DP is more sensitive to WSL as that by QLF, disregarding whether the automatic analysis or the experts' manual assessment of QLF is applied, and (ii) detected lesions in QLF are included in those of DP, were confirmed and not confirmed, respectively.
DP and QLF are valuable methods to detect WSL in demineralized teeth. Combining both modalities can provide additional information on early lesion assessment.
Objective
Hard tooth tissue demineralisation is an undesirable side effect of orthodontic treatment with fixed appliances. Whereas both clinically and in digital photographs (DP), demineralisations ...appear as white spot lesions, WSLs appear as dark areas when quantitative light-induced fluorescence (QLF) imaging is used. This study aims at comparing the reproducibility of the detection of decalcified tooth areas in DP and QLF.
Materials and methods
DP and QLF pairs were acquired from 139 teeth of 32 patients after braces removal. Three raters manually marked the decalcified area on both DP and QLF images. The markings were repeated after 2 weeks. A ground truth was estimated for each tooth and modality using the simultaneous truth and performance level estimation (STAPLE) algorithm. The Dice coefficients (DC) of each rater marking to the ground truth were calculated for all teeth and modalities to quantify the spatial agreement. A three-way repeated measures analysis of variance (ANOVA) was used to compare the means of the DCs for both modalities (
p
<
0.05
). Intra-observer and intercycle variabilities were assessed comparing the means across the raters and the cycles for both modalities.
Results
ANOVA revealed a statistical significant difference between the modalities
F
(
1
,
138
)
=
62.89
,
p
<
0.001
. The standard deviation of the DC for the photographs are lower than those for the QLF images. Intra-observer and intercycle differences are rather small as compared to the intermodality differences.
Conclusions
The results indicate a higher spatial reproducibility in identifying a decalcified area on a tooth surface using visual inspection of DP rather than QLF images.
Background: Asthma is a complex disease characterized by a high prevalence of allergic diathesis and the almost ubiquitous presence of upper airway disease (eg, rhinitis). Previously, we observed ...linkage of asthma among Afro-Caribbean families to markers in chromosome 12q, which contains a number of genes encoding for products closely related to allergic airway inflammation and disease.
Objective: To identify susceptibility loci in chromosome 12q contributing to the genetics of upper and lower airway diseases and to expand the region to include genes encoding IFN-γ (
IFNG ) and one of the signal transducers and activators of transcription (
STAT6 ), we conducted further linkage studies among 33 multiplex families.
Methods: We characterized 528 subjects from Barbados for asthma; 82% were characterized for allergic rhinitis. Two-point and multipoint linkage analysis of 22 microsatellite markers (spanning ~79 centimorgan) was performed.
Results: Affected sib-pair analysis revealed significant evidence for linkage to asthma over approximately 30 cM (
P < .05 to .002), with the best evidence for linkage at a CA repeat polymorphism in the first intron of
IFNG in 12q21.1 (
P = .002). Evidence of linkage to allergic rhinitis was observed in the same region (
D12S313 ,
P = 0.006, and
IFNGCA ,
P = .01, respectively). Multipoint linkage analysis also provided evidence for linkage to asthma, with the best nonparametric linkage analysis score at
D12S326 (nonparametric linkage score = 3.8,
P = .0008). Modest evidence for linkage to allergic rhinitis was observed next to
D12S326 at
D12S1052 (
P = .036).
Conclusions: Our findings suggest that (1) one or more loci in the chromosome 12q13.12–q23.3 region are contributing to the expression of the clinical phenotype asthma and the strongest evidence for linkage is in a region near the gene encoding
IFNG and (2) a susceptibility locus for both asthma and allergic rhinitis maps to this region. (J Allergy Clin Immunol 1999;104:485-91.)
Initial genome-wide scan data provided suggestive evidence for linkage of the asthma phenotype in African-American (AA), but not Caucasian, families to chromosome 11q markers (peak at D11S1985; ...LOD=2). To refine this region, mapping analysis of 91 AA families (51 multiplex families and 40 asthmatic case-parent trios) was performed with an additional 17 markers flanking the initial peak linkage marker. Multipoint analyses of the 51 multiplex families yielded significant evidence of linkage with a peak non-parametric linkage score of 4.38 at marker D11S1337 (map position 68.6 cM). Furthermore, family-based association and transmission disequilibrium tests conducted on all 91 families showed significant evidence of linkage in the presence of disequilibrium for several individual markers in this region. A putative susceptibility locus was estimated to be at map position 70.8 cM with a confidence interval spanning the linkage peak. Evidence from both linkage and association analyses suggest that this region of chromosome 11 contains one or more susceptibility genes for asthma in these AA families.
Background:
Dermatophagoides pteronyssinus (Der p) is one of the most frequently implicated allergens in atopic diseases. Although HLA could play an important role in the development of the IgE ...response to the Der p allergens, genetic regulation by non-
HLA genes influences certain HLA-associated IgE responses to complex allergens.
Objective: To clarify genetic control for the expression of Der p–specific IgE responsiveness, we conducted a genome-wide search for genes influencing Der p–specific IgE antibody levels by using 45 Caucasian and 53 African American families ascertained as part of the Collaborative Study on the Genetics of Asthma (CSGA).
Methods: Specific IgE antibody levels to the Der p crude allergen and to the purified allergens Der p 1 and Der p 2 were measured. Multipoint, nonparametric linkage analysis of 370 polymorphic markers was performed with the GENEHUNTER program.
Results: The best evidence of genes controlling specific IgE response to Der p was obtained in 2 novel regions: chromosomes 2q21-q23 (
P = .0033 for Caucasian subjects) and 8p23-p21 (
P = .0011 for African American subjects). Three regions previously proposed as candidate regions for atopy, total IgE, or asthma also showed evidence for linkage to Der p–specific IgE responsiveness: 6p21 (
P = .0064) and 13q32-q34 (
P = 0.0064) in Caucasian subjects and 5q23-q33 (
P = 0.0071) in African American subjects.
Conclusions: No single locus generated overwhelming evidence for linkage in terms of established criteria and guidelines for a genome-wide screening, which supports previous assertions of a heterogeneous etiology for Der p–specific IgE responsiveness. Two novel regions, 2q21-q23 and 8p23-p21, that were identified in this study merit additional study. (J Allergy Clin Immunol 1998;102:436-42.)
Both a functional promoter polymorphism in the gene encoding CD14 (C-260T) and exposure to endotoxin are believed to play key roles in modulating the immune response and expression of atopic disease.
...We aimed to evaluate the role of the CD14 C-260T polymorphism in a population of African descent and to test for interaction between this genotype and house dust endotoxin (HDE) exposure on atopic phenotypes.
Asthmatic probands and their families were recruited as part of the Barbados Asthma Genetics Study. The C-260T polymorphism and two additional
CD14 promoter markers (G-1461T, C-1721T) were genotyped. Endotoxin was measured in house dust samples.
Using a Family-Based Association Test, the C-260T allele appeared to be protective against asthma (
z
=
−2.444;
P
=
.015) and asthma severity (
z
=
−2.615;
P
=
.009) under a recessive model. No significant associations were observed for the G-1461T and C-1721T markers both individually and in haplotypes. In a case-control analysis, the CD14 TT genotype was found to reduce risk of asthma compared with the CD14 CC/CT genotypes (odds ratio OR, 0.26; 95% CI, 0.14-0.49) and was associated with lower asthma severity scores (
P < .002). The TT genotype might protect against asthma for individuals with low HDE (OR, 0.09; 95% CI, 0.03-0.24), but may be a risk factor for individuals with high HDE (OR, 11.66; 95% CI, 1.03-131.7), suggesting a gene-environment interaction.
These data suggest that the CD14-260 polymorphism may play a role in controlling risk to atopic disease and underscore the importance of incorporating key environmental exposures into studies of genetic risk factors.
Molecular biomarkers validated previously in animal models are increasingly being studied in conjunction with traditional clinical endpoints in therapeutic trials.
We hypothesized that human kidneys ...would exhibit a brisk, gene-specific inflammatory response during ischemia reperfusion injury (IRI), which would be modified by anti-adhesive therapy. Forty deceased-donor kidneys were biopsied prior to implantation and ∼1 h after reperfusion during an intervention trial with the selectin antagonist YSPSL (recombinant P-selectin glycoprotein ligand Ig). Ten inflammatory genes were measured by RT-PCR and normalized to three housekeeping genes.
Pre-implantation kidney biopsies were already significantly inflamed relative to healthy tissue, with transcripts encoding IL-6, IL-8, and CD25 > 10-fold elevated. After reperfusion, IL-6 and IL-8 increased additional 60- and 120-fold (p < 0.05), while already elevated CD25-levels remained stable. Furthermore, transcripts encoding MCP-1, E-selectin, and TNFα were also induced significantly upon reperfusion (p < 0.0005). Systemic treatment of the recipient with YSPSL pre-reperfusion, with or without pre-implantation YSPSL flush of the donor organ, attenuated the post-reperfusion increase in MCP-1 and TGFβ (p < 0.05), E-selectin and hemoxygenase 1 transcripts (p < 0.1).
Our data in humans demonstrate a robust increase in inflammatory gene transcript levels during kidney transplantation IRI and reduction thereof by inhibition of leukocyte adhesion.
Background: Allergic diseases are one of the major causes of morbidity in the developed countries today, and the prevalence of these diseases is increasing steadily. Study of total serum gE level is ...important in understanding the genetics of allergic iseases because IgE levels are considered to be a crucial pathogenic component. IL-13 plays an important role in the induction of IgE synthesis and in the pathogenesis of allergic diseases. Objective: We sought to examine potential variation at the IL13 gene and estimate its effect on elevated IgE level and atopic dermatitis (AD). Methods: We conducted mutational analyses of the IL13 gene by using single-stranded conformation polymorphism and DNA sequencing. Case control studies for high-IgE phenotype and AD were performed by using subjects from the German MAS-90 cohort. Results: A novel IL13 coding region variant at 4257 bp (G to A, fourth exon) was identified. Case control studies of a German sample from the MAS-90 cohort showed significant associations between the presence of the A allele and two atopic phenotypes: high IgE (odds ratio, 2.38; 95% confidence interval, 1.35-4.21; P = .0026) and AD (odds ratio, 1.77; 95% confidence interval, 1.06-2.96; P = .03). Conclusion: This IL13 coding region variant may be involved in the pathogenesis of AD and high total serum IgE level in a study population of white subjects. (J Allergy Clin Immunol 2000;106:167-70.)
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