ABSTRACT
BACKGROUND: The majority of complete dentures are still conventionally manufactured using a flask-and-pack technique. However, the polymerization process may introduce a distortion of the denture body. The aim of this study was to evaluate the three-dimensional fit of the posterior palatal seal of maxillary complete dentures with the original impression, and to give recommendations for scraping. METHODS: Four autopolymerising resins were used to manufacture 40 palatal plates each for high, medium and flat palates (total n = 120). The misfit was captured by taking a reline impression with a highly fluid silicone, the dimensions of which were measured with a flat-bed scanner. RESULTS: The shape of the palate had a significant impact (median p = 0.0435), but not the resin type (median p = 0.2575). It was largest for the flat palate and smallest for the high palate. The largest misfit was observed in the palatal midline area (flat-palate average median: 685 µm; high and medium palates: 620 µm) decreasing towards the lateral and anterior regions. CONCLUSIONS: The results suggest compensating for the palatal misfit that occurs with autopolymerising resins by scraping a postdam of an approximately 0.7 mm depth to the master cast, decreasing towards the anterior and lateral areas. In high and medium palates, the scraping could be less pronounced.
ABSTRACT
Short stature, with an incidence of 3 in 100, is a fairly frequent disorder in children. Idiopathic short stature refers to patients who are short due to various unknown reasons. Mutations of a human homeobox gene, SHOX (short stature homeobox), have recently been shown to be associated with the short stature phenotype in patients with Turner syndrome and most patients with Léri-Weill dyschondrosteosis. This study addresses the question of the incidence and type of SHOX mutations in patients with short stature. We analyzed the SHOX gene for intragenic mutations by single strand conformation polymorphism, followed by sequencing, in 750 patients and for complete gene deletions by fluorescence in situ hybridization in 150 patients (total, 900 patients). This is the largest group of patients with short stature studied to date for SHOX mutations. All patients had a normal karyotype, and their height for chronological age were below the third percentile or minus 2 SD of national height standards. All were without obvious skeletal features reminiscent of the Leri-Weill syndrome at the time of diagnosis. Silent, missense, and nonsense mutations and a small deletion in the coding region of SHOX were identified in 9 of the 750 patients analyzed for intragenic mutations. Complete gene deletions were detected in 3 of the 150 patients studied for gene deletions. At least 3 of the 9 intragenic mutations were judged to be functional based upon the genotype- phenotype relationship for the parents and normal control individuals. We conclude that SHOX mutations have been detected in 2.4% of children with short stature. The spectrum of SHOX mutations is biased, with the vast majority leading to complete gene deletions. The prevalence of short stature due to SHOX gene mutations among children with short stature appears to be similar to that of GH deficiency or Turner syndrome. Family studies of the children with SHOX mutations often reveal older family members with same mutation who exhibit mild skeletal features reminiscent of the Turner syndrome, such as high-arched palate, short neck, abnormal auricular development, cubitus valgus, genu valgum, short fourth metacarpals, and Madelung deformity.
