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1.
Artículo | IMSEAR | ID: sea-216844

RESUMEN

Aim: The aim of this study was to evaluate the dental arch spatial changes in maxillary and mandibular arches after premature loss of primary molars. Introduction: Primary teeth must be maintained during the change from primary to mixed and then permanent dentition, to preserve and maintain the dental arch. When this normal process is disturbed, usually due to severe decay requiring extraction before normal exfoliation, it can result in migration of adjacent teeth toward the missing space resulting in decreased arch length and malocclusion in the permanent dentition. Materials and Methods: A comprehensive search was conducted using electronic databases such as PubMed Central, Cochrane Database of Systematic Reviews, Google Scholar, LILACS, and ScienceDirect. The title and abstract were screened to find relevant articles, which were then reviewed in full to see if they were worthy of inclusion. All longitudinal and observational studies that looked at space changes after the loss of primary first or second molars were included. Quality assessment of the studies was done based on the Newcastle-Ottawa scale as all the included studies were non-randomized studies. Results: Four thousand five hundred and seventy-eight articles were identified by screening electronic database and assessed for eligibility, 12 full-text articles were assessed, and 4 full-text articles were excluded as they did not match the inclusion criteria. Thus, eight articles were included in this systematic review. Short term and long term space changes and loss of maxillary and mandibular molars were studied individually. In the short term changes, the distal migration of the primary cuspid towards the missing space within 1 month was attributable to early space changes after premature loss of the mandibular first molar, and the greatest space loss was recorded in the first 3 months after premature loss. After the premature loss of the maxillary first molar, immediate space loss of 1mm was documented due to distal migration of the primary canine. Studies found that space loss was caused by the distal migration of primary canines in the case of mandibular primary first molar loss, and that space loss was larger in the mandibular arch after premature loss of second primary molars. Conclusion: The greatest repercussions occurred during the first 3 months after the deciduous molars were extracted, and a space maintainer was recommended in the majority of cases, mainly when there is premature loss of mandibular second primary molar as it leads to mesial displacement of the first permanent molar.

2.
Chinese Journal of Stomatology ; (12): 851-854, 2019.
Artículo en Chino | WPRIM | ID: wpr-800043

RESUMEN

Space reduction after the premature loss of the second primary molars is one of the important factors affecting the occurrence of malocclusion, often increasing the demand for orthodontic treatment. It has great significance to select and apply appropriate appliances to maintainthe space soon after the premature loss of the second primary molars. The space should be maintained until the adjacent teeth and the successors erupt successfully. This review summarizes the selection and clinical application of the space maintainer for the premature loss of the second primary molars in different periods, to improve dentists′ awareness of the importance of space maintainers and to provide advises for clinical choices.

3.
Actual. osteol ; 14(1): 36-43, Ene - Abr. 2018. ilus
Artículo en Español | LILACS | ID: biblio-1116899

RESUMEN

La hipofosfatasia (HP) es una enfermedad congénita, causada por mutaciones con pérdida de función en el gen ALPL que codifica la isoenzima no específica de tejido de la fosfatasa alcalina (TNSALP). Su expresión clínica es muy variable, desde casos de muerte intraútero por alteración grave de la mineralización ósea, hasta casos solo con caída prematura de la dentición. Se presenta el caso clínico de un varón al que se le diagnosticó odontohipofosfatasia a los 30 meses por pérdida temprana de piezas dentarias y niveles anormalmente bajos de fosfatasa alcalina, sin signos de raquitismo ni deformidades óseas. Durante su seguimiento, hasta los 13 años, presentó síntomas compatibles con HP infantil leve, como cansancio al caminar, incoordinación en la marcha y dolor en miembros inferiores que aumentaban con la actividad física. Ante la aparición de edema bimaleolar y poca respuesta al tratamiento con calcitonina y antiinflamatorios, se descartaron patologías infecciosas o reumáticas o ambas y se diagnosticó, por biopsia de tibia y peroné, periostitis sin detección de cristales de pirofosfato. Los controles radiológicos durante su evolución mostraron ensanchamiento metafisario en muñeca, falta de remodelado de metacarpianos, hojaldrado perióstico en tibia y peroné e hipomineralización en metáfisis tibiales, con "lenguas radiolúcidas" características de HP. Como conclusión, la hipofosfatasia debe considerarse como una entidad clínica para descartar en niños que presentan pérdida temprana de dientes. La presencia de este cuadro clínico es en general suficiente para realizar el diagnóstico de HP de la niñez. (AU)


Hypophosphatasia (HP) is a congenital disease, caused by mutations with loss of function in the gene ALPL that encodes the non-specific tissue isoenzyme of alkaline phosphatase (TNSALP). Its clinical expression displays considerable variability, from cases of intrauterine death due to severe alteration of bone mineralization, to cases with only early loss of teeth. We report the case of a male, diagnosed as odontohypophosphatasia at 30 months of age due to early loss of teeth and abnormally low levels of alkaline phosphatase, without signs of rickets or bone deformities. During follow-up, up to 13 years of age, he presented symptoms consistent with mild infantile HP such as tiredness when walking, lack of gait coordination, and pain in lower limbs, especially after physical activity. Due to the appearance of bimalleolar edema and poor response to treatment with calcitonin and anti-inflammatory drugs, infectious and / or rheumatic pathologies were ruled out. Periostitis without pyrophosphate crystal detection was diagnosed by tibial and fibular biopsy. Radiological controls during follow up showed metaphyseal wrist enlargement, lack of remodeling of metacarpals, periosteal flaking in the tibia and fibula and hypomineralization in the tibial metaphysis, with "radiolucent tongues"; characteristic of HP. In conclusion, hypophosphatasia should be considered as a clinical entity in children who present early loss of teeth. The presentation of this clinical case is generally sufficient to make the diagnosis of childhood HP. (AU)


Asunto(s)
Humanos , Masculino , Preescolar , Niño , Adolescente , Fosfatasa Alcalina/genética , Hipofosfatasia/diagnóstico , Periostitis/diagnóstico , Trastorno por Déficit de Atención con Hiperactividad/diagnóstico , Trastorno por Déficit de Atención con Hiperactividad/terapia , Fluoruro de Sodio/administración & dosificación , Tibia/diagnóstico por imagen , Anomalías Dentarias/genética , Complejo Vitamínico B/uso terapéutico , Calcitonina/administración & dosificación , Carbamazepina/uso terapéutico , Fosfatasa Alcalina/sangre , Peroné/diagnóstico por imagen , Hidroxicolecalciferoles/efectos adversos , Hipofosfatasia/patología , Hipofosfatasia/sangre , Hipofosfatasia/terapia , Sulfato de Magnesio/uso terapéutico , Antiinflamatorios/uso terapéutico
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