36 research outputs found
Transmission of Curing Light through Moist, Air-Dried, and EDTA Treated Dentine and Enamel
Objective. This study measured light transmission through enamel and dentin and the effect of exposed dentinal tubules to light propagation. Methods. Light attenuation through enamel and dentin layers of various thicknesses (1 mm, 2 mm, 3 mm, and 4 mm) was measured using specimens that were (1) moist and (2) air-dried (n = 5). Measurements were repeated after the specimens were treated with EDTA. Specimens were transilluminated with a light curing unit (maximum power output 1869 mW/cm(2)), and the mean irradiance power of transmitting light was measured. The transmission of light through teeth was studied using 10 extracted intact human incisors and premolars. Results. Transmitted light irradiance through 1 mm thick moist discs was 500 mW/cm(2) for enamel and 398 mW/cm(2) for dentin (p < 0.05). The increase of the specimen thickness decreased light transmission in all groups (p < 0.005), and moist specimens attenuated light less than air-dried specimens in all thicknesses (p < 0.05). EDTA treatment increased light transmission from 398 mW/cm(2) to 439 mW/cm(2) (1 mm dentin specimen thickness) (p < 0.05). Light transmission through intact premolar was 6.2 mW/cm(2) (average thickness 8.2 mm) and through incisor was 37.6 mW/cm(2) (average thickness 5.6 mm). Conclusion. Light transmission through enamel is greater than that through dentin, probably reflecting differences in refractive indices and extinction coefficients. Light transmission through enamel, dentin, and extracted teeth seemed to follow Beer-Lambert's law
Dental Occlusion in a Split Amazon Indigenous Population: Genetics Prevails over Environment
Background: Studies examining human and nonhuman primates have supported the hypothesis that the recent increase in
the occurrence of misalignment of teeth and/or incorrect relation of dental arches, named dental malocclusion, is mainly
attributed to the availability of a more processed diet and the reduced need for powerful masticatory action. For the first
time on live human populations, genetic and tooth wear influences on occlusal variation were examined in a split
indigenous population. The Arara-Iriri people are descendants of a single couple expelled from a larger village. In the
resultant village, expansion occurred through the mating of close relatives, resulting in marked genetic cohesion with
substantial genetic differences.
Methodology/Principal Findings: Dental malocclusion, tooth wear and inbreeding coefficient were evaluated. The sample
examined was composed of 176 individuals from both villages. Prevalence Ratio and descriptive differences in the
outcomes frequency for each developmental stage of the dentition were considered. Statistical differences between the
villages were examined using the chi-square test or Fisher’s exact statistic. Tooth wear and the inbreeding coefficient (F)
between the villages was tested with Mann-Whitney statistics. All the statistics were performed using two-tailed distribution
at p#0.05. The coefficient inbreeding (F) confirmed the frequent incestuous unions among the Arara-Iriri indigenous group.
Despite the tooth wear similarities, we found a striking difference in occlusal patterns between the two Arara villages. In the
original village, dental malocclusion was present in about one third of the population; whilst in the resultant village, the
occurrence was almost doubled. Furthermore, the morphological characteristics of malocclusion were strongly different
between the groups.
Conclusions/Significance: Our findings downplay the widespread influence of tooth wear, a direct evidence of what an
individual ate in the past, on occlusal variation of living human populations. They also suggest that genetics plays the most
important role on dental malocclusion etiology
Genetic aspects of dental disorders
The document attached has been archived with permission from the Australian Dental Association. An external link to the publisher’s copy is included.This paper reviews past and present applications of quantitative and molecular genetics to dental disorders. Examples are given relating to craniofacial development (including malocclusion), oral supporting tissues (including periodontal diseases) and dental hard tissues (including defects of enamel and dentine as well as dental caries). Future developments and applications to clinical dentistry are discussed. Early investigations confirmed genetic bases to dental caries, periodontal diseases and malocclusion, but research findings have had little impact on clinical practice. The complex multifactorial aetiologies of these conditions, together with methodological problems, have limited progress until recently. Present studies are clarifying previously unrecognized genetic and phenotypic heterogeneities and attempting to unravel the complex interactions between genes and environment by applying new statistical modelling approaches to twin and family data. linkage studies using highly polymorphic DNA markers are providing a means of locating candidate genes, including quantitative trait loci (QTL). In future, as knowledge increases: it should be possible to implement preventive strategies for those genetically-predisposed individuals who are identified-predisposed individuals who are identified to be at risk.Grant C. Townsend, Michael J. Aldred and P. Mark Bartol
Extending Epigenesis: From Phenotypic Plasticity to the Bio-Cultural Feedback
The paper aims at proposing an extended notion of epigenesis acknowledging an actual causal import to the phenotypic dimension for the evolutionary diversification of life forms. Section 1 offers introductory remarks on the issue of epigenesis contrasting it with ancient and modern preformationist views. In Section 2 we propose to intend epigenesis as a process of phenotypic formation and diversification a) dependent on environmental influences, b) independent of changes in the genomic nucleotide sequence, and c) occurring during the whole life span. Then, Section 3 focuses on phenotypic plasticity and offers an overview of basic properties (like robustness, modularity and degeneracy) that allows biological systems to be evolvable – i.e. to have the potentiality of producing phenotypic variation. Successively (Section 4), the emphasis is put on environmentally-induced modification in the regulation of gene expression giving rise to phenotypic variation and diversification. After some brief considerations on the debated issue of epigenetic inheritance (Section 5), the issue of culture (kept in the background of the preceding sections) is considered. The key point is that, in the case of humans and of the evolutionary history of the genus Homo at least, the environment is also, importantly, the cultural environment. Thus, Section 6 argues that a bio-cultural feedback should be acknowledged in the “epigenic” processes leading to phenotypic diversification and innovation in Homo evolution. Finally, Section 7 introduces the notion of “cultural neural reuse”, which refers to phenotypic/neural modifications induced by specific features of the cultural environment that are effective in human cultural evolution without involving genetic changes. Therefore, cultural neural reuse may be regarded as a key instance of the bio-cultural feedback and ultimately of the extended notion of epigenesis proposed in this work
Considerações para elaboração de protocolo de assistência ortodôntica em saúde coletiva
Prevalência de oclusopatia na dentição decídua e permanente de crianças na cidade de São Paulo, Brasil, 1996
Taurodontism and the Presence of an Extra Y Chromosome: Study of 47,XYY Males and Analytical Review
A sample o f 47,XYY males was examined for taurodontism to provide further inform ation on the effects of chromosom eaneuploidies on the trait. The etiology of taurodontism is reviewed in light of recent findings. Two models have been put forward to explain the association of taurodontism with chromosome abnormalities: (1) Taurodontism results from a generalized disruption of developmental homeostasis, and (2) the development of taurodontism reflects a more specific action of the genes. The recent findings in 45,X females indicate that this chromosome aneuploidy does not have any effect on the development of taurodontism, in contrast to the findings of increased frequency of the trait in individuals with extra X chromosomes. The present results in 47,XYY males suggest that the presence of an extra Y chromosome does not cause an increase in the expression of taurodontism. It is concluded that the observed variation in the occurrence of taurodontism in individuals with sex chromosomes aneuploidies does not corroborate the hypothesis of disrupted homeostasis. Instead, the findings indicate that more specific action of gene(s) on the X chromosome is involved. We suggest that the effect of the Y chromosome on growth of both enamel and dentin, possibly in a regulative way, could be involved in the balanced growth of dental structures in 47,XYY males
Transmission of Curing Light through Moist, Air-Dried, and EDTA Treated Dentine and Enamel
Objective. This study measured light transmission through enamel and dentin and the effect of exposed dentinal tubules to light propagation. Methods. Light attenuation through enamel and dentin layers of various thicknesses (1 mm, 2 mm, 3 mm, and 4 mm) was measured using specimens that were (1) moist and (2) air-dried (n=5). Measurements were repeated after the specimens were treated with EDTA. Specimens were transilluminated with a light curing unit (maximum power output 1869 mW/cm2), and the mean irradiance power of transmitting light was measured. The transmission of light through teeth was studied using 10 extracted intact human incisors and premolars. Results. Transmitted light irradiance through 1 mm thick moist discs was 500 mW/cm2 for enamel and 398 mW/cm2 for dentin (p<0.05). The increase of the specimen thickness decreased light transmission in all groups (p<0.005), and moist specimens attenuated light less than air-dried specimens in all thicknesses (p<0.05). EDTA treatment increased light transmission from 398 mW/cm2 to 439 mW/cm2 (1 mm dentin specimen thickness) (p<0.05). Light transmission through intact premolar was 6.2 mW/cm2 (average thickness 8.2 mm) and through incisor was 37.6 mW/cm2 (average thickness 5.6 mm). Conclusion. Light transmission through enamel is greater than that through dentin, probably reflecting differences in refractive indices and extinction coefficients. Light transmission through enamel, dentin, and extracted teeth seemed to follow Beer-Lambert’s law
Effect of Removal of Enamel on Rebonding Strength of Resin Composite to Enamel
Objective. To examine the effect of removing the surface layer of enamel on the rebonding strength of resin composite. Methods. Teeth in four groups (n=10) were etched, a small amount of resin composite was bonded and debonded, then specimens in three groups were ground for different lengths of time (10 s, 20 s, 30 s) to remove an increasing amount of enamel, one group was left untouched. The teeth were bonded again and the bond strengths of 1st and 2nd bonding were compared and analysed against the amount of enamel loss in different groups (7 µm (±2); 12 µm (±1); 16 µm (±3)). Specimens were examined with SEM and by noncontacting optical profilometer. Results. Although results indicated higher rebonding strength with increasing enamel removal ANOVA showed low statistical differences between the groups (p>0.05). However, values between first bonding and rebonding strengths differed significantly (p<0.05) in the group that was not ground. SEM revealed that enamel-surfaces that were ground after debonding etched well, compared to the surfaces that still contained adhesive remnants. Conclusions. Removal of small amount of enamel refreshed the surface for rebonding. Rebonding strengths without grinding the surface before bonding were lower than bond strength to intact enamel