A photographic system for the three-dimensional study of facial morphology.

Abstract Objectives: To test whether digital photographs supported by three-dimensional (3D) software are suitable for measuring the facial soft tissues of healthy subjects as compared with data obtained by a certified 3D computerized electromagnetic digitizer. Materials and Methods: Three-dimensional soft tissue facial landmarks were obtained from the faces of 15 healthy young adults, using a 3D computerized electromagnetic digitizer and a new low-cost photogrammetry system. Twelve linear and 18 angular measurements were computed. Errors between methods and repeatability of the new method were calculated. Results: Systematic errors between methods were found for only two distances and three angles (paired t-test, P < .05). The mean absolute differences between methods were always lower than 3 mm and 3 degrees. Repeated digitization of photographs showed that the method was repeatable (no systematic differences; random errors lower than 1.6 mm and 3 degrees). Repeated sets of photographs showed random errors of up to 5.3 mm and 5.6 degrees, without systematic biases. Conclusion: The 3D photogrammetry system can provide reliable facial measurements. The method is relatively fast and requires only inexpensive equipment. It is simple to use for private practice, research, or other practice

Analysis of tissue structure and remodeling ion alveolar ridges augmented with human palate or tuberosity mucosa

Previous clinical reports found different clinical outcomes of localized alveolar ridge augmentation with soft tissue harvested either from the palate or from the tuberosity over time, showing that the palatal grafts had a better tissue stability than those from the tuberosity, which tended to a hyperplastic reaction. The mechanisms responsible for a different maturation of the grafted tissue using the two donor sites are still unclear, very likely depending on differences of the structure and extracellular matrix of connective tissue (CT). The current study aimed at comparing the morphology and collagen turnover-related molecular pathways of sites grafted with CT from either the palate (group A = 7 patients) or the tuberosity (group B = 7 patients) one year after surgical procedures for ridge augmentation. Cultured fibroblasts were obtained to analyze by real-time PCR the mRNA levels for collagen type I and III (COL-I, COL-III), matrix metalloproteinases (MMP-1 and 2), long lysyl hydroxylase 2b (LH2b). Collagen protein levels were assessed by slot blot, collagen degradation by SDS-zymography. No significant differences in collagen content were found. COLI and III, MMP-1 and 2 expression was similar in cell culture supernatants from palate and tuberosity fibroblasts, although COL-I and COL-III protein levels resulted up-regulated, respectively, in 57% and 66% of the samples. LH2b/COL-I mRNA ratio 69% was higher in the tuberosity fibroblasts, suggesting that the tuberosity collagen could be cross-linked at a higher extent, and therefore less susceptible to degradation by MMPs, leading to its excessive accumulation. Our data show that in group B the higher LH2b/COL-I mRNA ratio may be responsible for differences in collagen maturation as the major determinants in the hyperplastic response, and that grafting using the maxillary tuberosity could avoid unwanted tissue contraction over time

Histological and immunohistochemical analysis of the bone-implant interface during early phases of osseointegration in different bone defects

The present study aimed to evaluate the histological features of bone healing around dental implants placed in bone defects of different sizes [1]. In the mandible of 12 Labrador dogs the premolar and molar teeth were extracted bilaterally. After 6 months of healing six implants were placed in two conventional sites, in two sites with a marginal gap of 0.5 mm (small defects) and in two sites with a marginal gap of 1.25 mm (large defects). Bone biopsies harvesting was scheduled in order to obtain healing times of 5, 10, 20 and 30 days. Before decalcification with EDTA was completed, mesial and distal cuts parallel to the long axis of the implant were made through the tissues and a buccal and lingual portion of the tissue block were separated from the implant. The soft tissue portions were dehydrated in ethanol, embedded in paraffin and sectioned with the microtome set at 7 μm. Mayer-Haematoxylin/Eosin was used to show the presence of the inflammatory infiltrate and to evaluate the percentage of newly formed microvessels at the different time points around the implants. Picrosirius Red was used to evaluate the collagen content while polarized light was used to enhance the birefringency of the staining and show collagen bundles distribution [2]. Immunohistochemistry with osteopontin (OPN) was performed to evaluate its distribution. In all groups, angiogenesis increased from 5 to 20 days and then decreased slightly. The collagen distribution had a similar behavior. In all defects, OPN expression increased until the 10th day, decreased at 20 days and then stabilized. Control sites showed a lower percentage of OPN compared to the sites with marginal gaps. The small defects showed the highest OPN concentration and the largest value of collagen content. Apparently a small marginal gap around the dental implant during the early phases of healing may accelerate bone regeneration

Identification of a new putative functional IL18 gene variant through an association study in systemic lupus erythematosus

Interleukin-18 (IL-18) is a proinflammatory cytokine that plays an important role in chronic inflammation and autoimmune disorders. In this study, we aimed to determine the potential role of the IL18 gene in SLE. To define the genetic association of the IL18 and SLE, we have genotyped nine SNPs in an independent set of Spanish cases and controls. The IL18 polymorphisms were genotyped by PCR, using a predeveloped TaqMan allele discrimination assay. Two SNPs were still significant after fine mapping of the IL18 gene. The SNP (rs360719) surviving correction for multiple tests was genotyped in two replication cohorts from Italy and Argentina. After the analysis, a significance with rs360719 C-allele remained across the sets and after the meta-analysis (Pooled OR 5 1.37, 95% CI 1.21-1.54, combined P 5 3.8E-07, Pc 5 1.16E-06). Quantitative real-time PCR was performed to assess IL18 mRNA expression in PBMC from subjects with different IL18 rs360719 genotypes. We tested the effect of the IL18 rs360719 polymorphism on the transcription of IL18 by electrophoretic mobility shift assay and western blot. We found a significant increase in the relative expression of IL18 mRNA in individuals carrying the rs360719 C-risk allele; in addition we show that the polymorphism creates a binding site for the transcriptional factor OCT-1. These findings suggest that the novel IL18 rs360719 variant may play an important role in determining the susceptibility to SLE and it could be a key factor in the expression of the IL18 gene. © The Author 2009. Published by Oxford University Press. All rights reserved

Kallikrein genes are associated with lupus and glomerular basement membrane-specific antibody-induced nephritis in mice and humans

Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that may be responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family, which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less evidence of disease. Antagonizing the kallikrein pathway augmented disease, while agonists dampened the severity of anti-GBM antibody-induced nephritis. In addition, nephritis-sensitive mouse strains had kallikrein haplotypes that were distinct from those of control strains, including several regulatory polymorphisms, some of which were associated with functional consequences. Indeed, increased susceptibility to anti-GBM antibody-induced nephritis and spontaneous lupus nephritis was achieved by breeding mice with a genetic interval harboring the kallikrein genes onto a disease-resistant background. Finally, both human SLE and spontaneous lupus nephritis were found to be associated with kallikrein genes, particularly KLK1 and the KLK3 promoter, when DNA SNPs from independent cohorts of SLE patients and controls were compared. Collectively, these studies suggest that kallikreins are protective disease-associated genes in anti-GBM antibody-induced nephritis and lupus

Genetic associations of leptin-related polymorphisms with systemic lupus erythematosus

Leptin is abnormally elevated in the plasma of patients with systemic lupus erythematosus (SLE), where it is thought to promote and/or sustain pro-inflammatory responses. Whether this association could reflect an increased genetic susceptibility to develop SLE is not known, and studies of genetic associations with leptin-related polymorphisms in SLE patients have been so far inconclusive. Here we genotyped DNA samples from 15,706 SLE patients and healthy matched controls from four different ancestral groups, to correlate polymorphisms of genes of the leptin pathway to risk for SLE. It was found that although several SNPs showed weak associations, those associations did not remain significant after correction for multiple testing. These data do not support associations between defined leptin-related polymorphisms and increased susceptibility to develop SLE