The heritability of malocclusion: Part 1--Genetics, principles and terminology.
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The relative contribution of genes and the environment to the aetiology of malocclusion has been a matter of controversy throughout the twentieth century. Genetic mechanisms are clearly predominant during embryonic craniofacial morphogenesis, but environment is also thought to influence dentofacial morphology postnatally, particularly during facial growth. Orthodontic and orthopaedic techniques are used in the treatment of malocclusion and other dentofacial deformities, but with limited effectiveness. The key to the determination of the aetiology of malocclusion, and its treatability lies in the ability to differentiate the effect of genes and environment on the craniofacial skeleton in a particular individual. Our ability to do this is limited by our lack of knowledge on the genetic mechanisms that control facial growth and lack of scientific evidence for the influence of environmental factors on human craniofacial morphogenesis. (+info)
Skeletal and dental changes following the use of the Frankel functional regulator.
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The purpose of this study was to assess the relative contributions of skeletal and dental components in correction of Class II division 1 malocclusions when treated with Frankel's functional regulator (FR). This was a retrospective study involving analyses of pre- and post-treatment cephalograms of 63 Class II division 1 patients treated with the FR to demonstrate the relative maxillary, mandibular, incisor, and molar movements during treatment compared with normal growth within a control group of untreated 39 Class II division 1 cases drawn from the same demographic population. All cephalograms were digitized and subjected to a Pitchfork analysis, which measured individual anteroposterior skeletal and dental changes during the period of study. It was shown that the FR was effective in treating Class II division 1 cases with the studied group being corrected to a clinically acceptable overjet and overbite of 2-3 mm. The majority of the correction came from dental movements, the most significant being the retroclination of the upper incisor teeth (mean 4.1 mm, 95 per cent CI +/- 0.44) and proclination of the lowers (mean 2.2 mm 95 per cent CI +/- 0.57). As regards skeletal correction, the most significant contribution was the restraint of normal maxillary forward growth (mean -0.2 mm, 95 per cent CI +/- 0.62) with forward mandibular growth not being a significant factor. (+info)
The many faces and factors of orofacial clefts.
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Orofacial clefts are congenital structural anomalies of the lip and/or palate that affect approximately 1/1000 live births. Their frequent occurrence as well as their extensive psychological, surgical, speech and dental involvement emphasize the importance of understanding the underlying causes. The etiology of orofacial clefts is complex, including multiple genetic and environmental factors. Rare forms, where they occur as one component of multiple congenital anomaly syndromes, have Mendelian or teratogenic origins; the non-syndromic forms of orofacial clefts are more common and are likely due to secondary gene-environment interactions. Recent advances in both molecular and quantitative approaches have begun to identify the genes responsible for the rare syndromic forms of cleft and have also identified both candidate genes and loci for the more common and complex non-syndromic variants. Animal models, in particular the mouse, have also contributed greatly to an understanding of these disorders. This review describes genes that are involved in orofacial clefts in humans and animal models and explores genetic approaches to identifying additional genes and gene-environment interactions that constitute the many factors of orofacial clefts. (+info)
Protein malnutrition affects the growth trajectories of the craniofacial skeleton in rats.
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To investigate the effects of protein malnutrition on a normal growth trajectory, we radiographed Rattus norvegicus from 22 d (weaning) and continuing past adult size. We took measurements from longitudinal radiographs of rats fed a control diet and littermates fed an isocaloric low protein experimental diet. A Gompertz model was fit to each individual rat for body weight and 22 measurements of the craniofacial skeleton, producing parameters that described the rate and timing of growth. We tested for differences in these parameters due to diet, sex and litter with a mixed-model three-way ANOVA. Allometric analysis examined the scaling relationships between and within various regions of the skull. For most measurements, final sizes predicted by the model were not significantly different between rats fed the two diets, although the differences in final measurements showed small, but significant differences in growth between rats in the two diet groups. The instantaneous initial rate of growth, maximum rate of growth and deceleration of growth were significantly higher in the control rats for every measurement. Rats fed the low protein diet grew for a significantly longer period of time. The shape of the neurocranium was relatively conserved between diet groups; however, rats fed the low protein diet had shorter and relatively wider skulls than the controls. These results suggest that functional demands of the viscerocranium were greater after birth, and that growth in this area was faster. The viscerocranium reached functional adult proportions earlier and was therefore more susceptible to epigenetic perturbations such as dietary protein level. Protein malnutrition did not affect many aspects of adult size, but strongly altered the growth trajectory to achieve that size. (+info)
Three-dimensional facial growth studied by optical surface scanning.
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The objective of the investigation was to study the three-dimensional growth of the face, and to examine the hypothesis that there are three-dimensional differences between the faces of boys and girls. The subjects comprised 132 British Caucasians aged 5-10 years measured by optical surface scanning in this cross-sectional study. Average scans for each age and sex subgroup were superimposed to assess the differences with age and sex. Males were generally larger than females. The greatest difference was between the facial heights and the least in the mid-facial dimensions. The face height of both sexes increased by an average of 3-4 mm annually. Mid-face prominence and width altered little. Mandibular width increased by 1-3 mm a year, rising to 3-5 mm in some years at the inferior areas of the mandibular region. Mandibular prominence also increased. Nose height and prominence and alar base width increased by 2 mm per year on average. Dorsum width changed little. Boys were generally larger than girls. Growth in facial height was greatest. Mid-face prominence and width changed little with age, whilst the prominence and width of the lower face increased more. Nasal prominence and alar base width increased at most ages. Dimensions changed more than reported by cephalometric studies, possibly as this study included the soft tissues. Refereed Scientific Paper (+info)
Comparison of mandibular morphology in Korean and European-American children with Class III malocclusions using finite-element morphometry.
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The purpose of this study was to determine whether the morphology of the mandible differed in subjects of diverse ethnic origin exhibiting Class III malocclusions. Lateral cephalographs of 147 children of either Korean or European-American descent aged between 5 and 11 years were compared. The cephalographs were subdivided into seven age- and sex-matched groups, traced, and eight mandibular homologous landmarks digitized. Average mandibular geometries, scaled to an equivalent size, were computed using Procrustes superimposition and subjected to ANOVA. Graphical analysis using a colour-coded finite element (FEM) programme was used to localize differences in morphology. Results indicated that the overall mean Korean and European-American mandibular configurations differed statistically (P < 0.001) and statistical difference was maintained at all age-wise comparisons. Comparing Korean and European-American Class III mandibular configurations for local size-change, FEM analysis revealed that the Korean condylar and mental regions generally were smaller (approximately 15-20 per cent decrease in size, respectively). However, an antero-posterior increase in the size of the mandibular corpus was most apparent in the incisor alveolus region (approximately 35 per cent increase in size). For shape-change, the Korean and European-American mandibular configurations were fairly isotropic except in the symphyseal and incisor alveolus regions. Dissimilarities in mandibular morphology are identifiable particularly in the dento-alveolar regions in subjects of diverse ethnic origin exhibiting Class III malocclusions. These differences may reflect genetic and/or environmental influences that might determine the severity and prevalence of the condition, and its subsequent clinical management. (+info)
Genetic and teratogenic approaches to craniofacial development.
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Craniofacial malformations are the most common birth defects that occur in humans, with facial clefting representing the majority of these defects. Facial clefts can arise at any stage of development due to perturbations that alter the extracellular matrix as well as affect the patterning, migration, proliferation, and differentiation of cells. In this review, we focus on recent advances in the understanding of the developmental basis for facial clefting through the analysis of the effects of gene disruption experiments and treatments with teratogens in both chickens and mice. Specifically, we analyze the results of disruptions to genes such as Sonic hedgehog (Shh), epidermal growth factor receptor (EGFR), Distal-less (Dlx), and transforming growth factor beta 3 (TGFbeta3). We also describe the effects that teratogens such as retinoic acid, jervine, and cyclopamine have on facial clefting and discuss mechanisms for their action. In addition to providing insight into the bases for abnormal craniofacial growth, genetic and teratogenic techniques are powerful tools for understanding the normal developmental processes that generate and pattern the face. (+info)
Construction for the modern head: current concepts in craniofacial development.
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The vertebrate head is a highly complex composite structure whose morphological characteristics are controlled at the level of the gene. There is now increasing evidence for the role of gene families that encode transcription factors in determining the embryonic plan of the developing craniofacial complex. These genes act as regulators of gene transcription being intimately involved with the control of complex interactions between multiple downstream genes. Combinatorial expression of the Hox genes (a family of highly conserved master regulatory genes related to the homeotic genes of the fruitfly Drosophila) have been shown to play a definitive role in patterning distinct regions of the craniofacial complex. In the vertebrate, Hox genes pattern the hindbrain and branchial regions of the developing head up to and including structures derived from the second branchial arch. The first branchial arch and more rostral regions of the head are patterned by groups of homeobox genes more diverged from the original Hox clusters. Transgenic mice, with targeted disruptions in many of these genes, are now providing insights into the molecular mechanisms that lie behind a number of craniofacial defects seen in man. (+info)