RESUMEN
This revised Clinical Guideline in Paediatric Dentistry replaces the previously published sixth guideline (Fayle SA. Int J Paediatr Dent 1999; 9: 311-314). The process of guideline production began in 1994, resulting in first publication in 1997. Each guideline has been circulated widely for consultation to all UK consultants in paediatric dentistry, council members of the British Society of Paediatric Dentistry (BSPD), and to people of related specialities recognized to have expertise in the subject. The final version of this guideline is produced from a combination of this input and thorough review of the published literature. The intention is to encourage improvement in clinical practice and to stimulate research and clinical audit in areas where scientific evidence is inadequate. Evidence underlying recommendations is scored according to the SIGN classification and guidelines should be read in this context. Further details regarding the process of paediatric dentistry guideline production in the UK is described in the Int J Paediatr Dent 1997; 7: 267-268.
Asunto(s)
Coronas , Caries Dental/terapia , Restauración Dental Permanente/normas , Odontología Pediátrica/normas , Diseño de Prótesis , Preescolar , Humanos , Diente Molar , Acero Inoxidable , Diente Primario , Reino UnidoRESUMEN
Amelogenesis imperfecta (AI) is a heterogeneous group of inherited disorders of defective enamel formation. The major protein involved in enamel formation, amelogenin, is encoded by a gene located at Xp22.1-Xp22.3. This study investigated the molecular defect producing a combined phenotype of hypoplasia and hypomineralization in a family with the clinical features and inheritance pattern of X-linked amelogenesis imperfecta (XAI). Genomic DNA was prepared from buccal cells sampled from family members. The DNA was subjected to the polymerase chain-reaction (PCR) in the presence of a series of oligonucleotide primers designed to amplify all 7 exons of the amelogenin gene. Cloning and sequencing of the purified amplification products identified a cytosine deletion in exon VI at codon 119. The deletion resulted in a frameshift mutation, introducing a premature stop signal at codon 126, producing a truncated protein lacking the terminal 18 amino acids. Identifying mutations assists our understanding of the important functional domains within the gene, and finding another novel mutation emphasizes the need for family-specific diagnosis of amelogenesis imperfecta.
Asunto(s)
Amelogénesis Imperfecta/genética , Proteínas del Esmalte Dental/genética , Aberraciones Cromosómicas Sexuales/genética , Cromosoma X , Amelogenina , Sustitución de Aminoácidos , Clonación Molecular , Citosina , Femenino , Mutación del Sistema de Lectura , Ligamiento Genético , Humanos , Masculino , Linaje , Reacción en Cadena de la Polimerasa , Análisis de Secuencia de ADN , Eliminación de Secuencia , TiminaRESUMEN
OBJECTIVE: Determination of the incidence of Candida carriage in patients with Sjögren's syndrome (SS) and xerostomic controls to assess the influence of immunologic disturbances in SS on carriage. STUDY DESIGN: A total of 16 primary SS patients, 12 secondary SS patients, and 14 xerostomic controls were included in the study. Sampling was performed using an oral rinse method. Aliquots (100 microliters) were spread onto CHROMagar* and incubated for 48 hours. Species identification was confirmed by the germ tube test and API ID32C. Total colony-forming units per milliliter (CFU/ml) were counted and statistical analyses performed by the Kruskal-Wallis test. RESULTS: Candida carriage in primary SS, secondary SS, and xerostomic patients was 81.25%, 66.7%, and 71.4%, respectively. There were no statistically significant differences in total CFU/ml. A wide range of species was isolated in each group. CONCLUSION: The immunologic disturbances seen in SS do not significantly influence the intraoral Candida carriage in patients with a dry mouth.