Orthodontic Treatment of a Congenitally Missing Maxillary Lateral Incisor

Clinicians agree that, regardless of gender or race, tooth agenesis has become more prominent in recent societies. The congenital absence of one or more maxillary lateral incisors poses a challenge to effective treatment planning for the restorative dentist. However, the one-sided orthodontic approach of just moving canines mesially to eliminate restorative procedures leads to compromise. Adult patients presenting with malocclusions, missing lateral incisors, or anterior crowding but who fail to get proper orthodontic treatment, requesting instead esthetic solutions that do not establish a stable occlusion, proper alignment, and proper axial inclination of the teeth will have compromised esthetic and periodontal results. An evaluation of anterior smile esthetics must include both static and dynamic evaluations of frontal and profile views to optimize both dental and facial appearance. This article presents how orthodontics is combined with other specialties in treating a congenitally missing lateral incisor. One case is used to illustrate how orthodontic treatment is progressed in collaboration with other specialists

Orthodontic treatment for deep bite and retroclined upper front teeth in children

Background A Class II division 2 malocclusion is characterised by upper front teeth that are retroclined (tilted toward the roof of the mouth) and an increased overbite (deep overbite), which can cause oral problems and may affect appearance. This problem can be corrected by the use of special dental braces (functional appliances) that move the upper front teeth forward and change the growth of the upper or lower jaws, or both. Most types of functional appliances are removable and this treatment approach does not usually require extraction of any permanent teeth. Additional treatment with fixed braces may be necessary to ensure the best result. An alternative approach is to provide space for the correction of the front teeth by moving the molar teeth backwards. This is done by applying a force to the teeth from the back of the head using a head brace (headgear) and transmitting this force to part of a fixed or removable dental brace that is attached to the back teeth. The treatment may be carried out with or without extraction of permanent teeth. If headgear use is not feasible, the back teeth may be held in place by bands connected to a fixed bar placed across the roof of the mouth or in contact with the front of the roof of the mouth. This treatment usually requires two permanent teeth to be taken out from the middle of the upper arch (one on each side). Objectives To establish whether orthodontic treatment that does not involve extraction of permanent teeth produces a result that is any different from no orthodontic treatment or orthodontic treatment involving extraction of permanent teeth, in children with a Class II division 2 malocclusion. Search methods Cochrane Oral Health's Information Specialist searched the following electronic databases: Cochrane Oral Health's Trials Register (to 13 November 2017), the Cochrane Central Register of Controlled Trials (CENTRAL) (the Cochrane Library, 2017, Issue 10), MEDLINE Ovid (1946 to 13 November 2017), and Embase Ovid (1980 to 13 November 2017). To identify any unpublished or ongoing trials, the US National Institutes of Health Ongoing Trials Register (ClinicalTrials.gov) and the World Health Organization International Clinical Trials Registry Platform (apps.who.int/trialsearch) were searched. We also contacted international researchers who were likely to be involved in any Class II division 2 clinical trials. Selection criteria Randomised controlled trials (RCTs) and controlled clinical trials (CCTs) of orthodontic treatments to correct deep bite and retroclined upper front teeth in children. Data collection and analysis Two review authors independently screened the search results to find eligible studies, and would have extracted data and assessed the risk of bias from any included trials. We had planned to use random-effects meta-analysis; to express effect estimates as mean differences for continuous outcomes and risk ratios for dichotomous outcomes, with 95% confidence intervals; and to investigate any clinical or methodological heterogeneity. Main results We did not identify any RCTs or CCTs that assessed the treatment of Class II division 2 malocclusion in children. Authors' conclusions There is no evidence from clinical trials to recommend or discourage any type of orthodontic treatment to correct Class II division 2 malocclusion in children. This situation seems unlikely to change as trials to evaluate the best management of Class II division 2 malocclusion are challenging to design and conduct due to low prevalence, difficulties with recruitment and ethical issues with randomisation

Velo-Cardio-Facial Syndrome: 30 Years of Study

Velo-cardio-facial syndrome is one of the names that has been attached to one of the most common multiple anomaly syndromes in humans. The labels DiGeorge sequence, 22q11 deletion syndrome, conotruncal anomalies face syndrome, CATCH 22, and Sedlačková syndrome have all been attached to the same disorder. Velo-cardio-facial syndrome has an expansive phenotype with more than 180 clinical features described that involve essentially every organ and system. The syndrome has drawn considerable attention because a number of common psychiatric illnesses are phenotypic features including attention deficit disorder, schizophrenia, and bipolar disorder. The expression is highly variable with some individuals being essentially normal at the mildest end of the spectrum, and the most severe cases having life-threatening and life-impairing problems. The syndrome is caused by a microdeletion from chromosome 22 at the q11.2 band. Although the large majority of affected individuals have identical 3 megabase deletions, less than 10% of cases have smaller deletions of 1.5 or 2.0 megabases. The 3 megabase deletion encompasses a region containing 40 genes. The syndrome has a population prevalence of approximately 1:2,000 in the United States, although incidence is higher. Although initially a clinical diagnosis, today velo-cardio-facial syndrome can be diagnosed with extremely high accuracy by fluorescence in situ hybridization and several other laboratory techniques. Clinical management is age dependent with acute medical problems such as congenital heart disease, immune disorders, feeding problems, cleft palate, and developmental disorders occupying management in infancy and preschool years. Management shifts to cognitive, behavioral, and learning disorders during school years, and then to the potential for psychiatric disorders including psychosis in late adolescence and adult years. Although the majority of people with velo-cardio-facial syndrome do not develop psychosis, the risk for severe psychiatric illness is 25 times higher for people affected with velo-cardio-facial syndrome than that of the general population. Therefore, interest in understanding the nature of psychiatric illness in the syndrome remains strong

Mapping cellular processes in the mesenchyme during palatal development in the absence of Tbx1 reveals complex proliferation changes and perturbed cell packing and polarity

The 22q11 deletion syndromes represent a spectrum of overlapping conditions including cardiac defects and craniofacial malformations. Amongst the craniofacial anomalies that are seen, cleft of the secondary palate is a common feature. Haploinsufficiency of TBX1 is believed to be a major contributor toward many of the developmental structural anomalies that occur in these syndromes, and targeted deletion of Tbx1 in the mouse reproduces many of these malformations, including cleft palate. However, the cellular basis of this defect is only poorly understood. Here, palatal development in the absence of Tbx1 has been analysed, focusing on cellular properties within the whole mesenchymal volume of the palatal shelves. Novel image analyses and data presentation tools were applied to quantify cell proliferation rates, including regions of elevated as well as reduced proliferation, and cell packing in the mesenchyme. Also, cell orientations (nucleus–Golgi axis) were mapped as a potential marker of directional cell movement. Proliferation differed only subtly between wild‐type and mutant until embryonic day (E)15.5 when proliferation in the mutant was significantly lower. Tbx1 (−/−) palatal shelves had slightly different cell packing than wild‐type, somewhat lower before elevation and higher at E15.5 when the wild‐type palate has elevated and fused. Cell orientation is biased towards the shelf distal edge in the mid‐palate of wild‐type embryos but is essentially random in the Tbx1 (−/−) mutant shelves, suggesting that polarised processes such as directed cell rearrangement might be causal for the cleft phenotype. The implications of these findings in the context of further understanding Tbx1 function during palatogenesis and of these methods for the more general analysis of genotype–phenotype functional relationships are discussed