In vitro effects of erosive challenge on the surface properties of sealants

Aim: To assess in vitro the surface roughness (Ra), Vickers hardness (VHN) and surface morphology of resin and glass ionomer materials used for sealants after dynamic erosive challenge. Methods: Twenty specimens of each material were prepared and divided into experimental (erosive challenge) and control groups (n=10): Protect Riva (SDI), Opallis Flow (3M ESPE), Fluroshield (Dentsply), Filtek Z350 XT Flow (3M ESPE). The erosive challenge was performed 4 times per day (90 s) in cola drink and for 2 h in artificial saliva for 7 days. The control specimens were maintained in artificial saliva. Ra and VHN readings were performed before and after erosion. The percentage of hardness loss (%VHN) was obtained after erosion. The surface morphology was evaluated by scanning electron microscopy (SEM). The data were analyzed by ANOVA, Tukey and paired t tests (α=0.05). Results: After erosion and saliva immersion, there was an increase in Ra values for all groups and Riva group showed the highest Ra values. After erosive challenge, Riva and Filtek groups showed significant decrease in VHN values, but Filtek group showed the greatest %VHN. For all groups there was inorganic particle protrusion and matrix degradation after erosion visualized by SEM images. Conclusions: Erosive challenge affected the surface properties of all materials used as sealants, particularly in the Riva and Filtek groups.

Erosive potential of sugar-free hard candies dissolved in water and artificial saliva

Aim: To compare the acidity of sugar-free hard candies dissolved in water and artificial saliva. Methods: Sugar-free Flopi Florestal hard candies (grape, strawberry, cherry, orange, ginger, lemon balm, fennel) were selected and grouped in 2 groups: G-1 (candies dissolved in distilled water) and G-2 (candies dissolved in artificial saliva). Candies were triturated with a porcelain pestle, yielding two samples of 20 g. Samples were dissolved in 120 mL distilled water (G-1) and 120 mL artificial saliva (20 mM NaHCO3, 3 mM NaH2PO4.H2O and 1 mM CaCl2.2H2O) (G-2), obtaining three samples of 30 mL for each of the flavors and groups. pH was measured using potentiometer and combined glass electrode. Titratable acidity was evaluated by adding 100 μL 1M NaOH aliquots until reaching pH 5.5. For statistical analysis, analysis of variance (ANOVA) was used. Means were compared by the Tukey test at 5% significance level (p<0.05) Results: All flavors of G-1 showed pH values below 5.5. Comparison of groups in the same flavor showed a significant increase in pH in flavors of G-2. Comparison of the titratable acidity between G-1 and G-2, showed that fruit flavors were significantly different from each other, with reduced acidity in G-2. Conclusions: All evaluated candies are acid, and dilution in artificial saliva raised their pH and lowered their titratable acidity, reducing their erosive potential.

Charcot Marie Tooth disease (CMT4A) due to GDAP1 mutation: report of a colombian family

Background: Mutations of GDAP1 gene cause autosomal dominant and autosomal recessive Charcot-Marie-Tooth disease and more than 40 different mutations have been reported. The recessive Q163X mutation has been described in patients of Spanish ancestry, and a founder mutation in South American patients, originating in Spain has been demonstrated. Objective: We describe physical and histological features, and the molecular impact of mutation Q163X in a Colombian family. Methods: We report two female patients, daughters of consanguineous parents, with onset of symptoms within the first two years of life, developing severe functional impairment, without evidence of dysmorphic features, hoarseness or diaphragmatic paralysis. Electrophysiology tests showed a sensory and motor neuropathy with axonal pattern. Sequencing of GDAP1 gene was requested and the study identified a homozygous point mutation (c.487 C>T) in exon 4, resulting in a premature stop codon (p.Q163X). This result confirms the diagnosis of Charcot-Marie-Tooth disease, type 4A. Results: The patients were referred to Physical Medicine and Rehabilitation service, in order to be evaluated for ambulation assistance. They have been followed by Pulmonology service, for pulmonary function assessment and diaphragmatic paralysis evaluation. Genetic counseling was offered. The study of the genealogy of the patient, phenotypic features, and electrophysiological findings must be included as valuable tools in the clinical approach of the patient with Charcot-Marie-Tooth disease, in order to define a causative mutation. In patients of South American origin, the presence of GDAP1 gene mutations should be considered, especially the Q163X mutation, as the cause of CMT4A disease.

Charcot Marie Tooth disease (CMT4A) due to GDAP1 mutation: report of a colombian family

Background: Mutations of GDAP1 gene cause autosomal dominant and autosomal recessive Charcot-Marie-Tooth disease and more than 40 different mutations have been reported. The recessive Q163X mutation has been described in patients of Spanish ancestry, and a founder mutation in South American patients, originating in Spain has been demonstrated. Objective: we describe physical and histological features, and the molecular impact of mutation Q163X in a Colombian family. Methods: We report two female patients, daughters of consanguineous parents, with onset of symptoms within the first two years of life, developing severe functional impairment, without evidence of dysmorphic features, hoarseness or diaphragmatic paralysis. Electrophysiology tests showed a sensory and motor neuropathy with axonal pattern. Sequencing of GDAP1 gene was requested and the study identified a homozygous point mutation (c.487 C>T) in exon 4, resulting in a premature stop codon (p.Q163X). This result confirms the diagnosis of Charcot-Marie-Tooth disease, type 4A. Results: The patients were referred to Physical Medicine and Rehabilitation service, in order to be evaluated for ambulation assistance. They have been followed by Pulmonology service, for pulmonary function assessment and diaphragmatic paralysis evaluation. Genetic counseling was offered. The study of the genealogy of the patient, phenotypic features, and electrophysiological findings must be included as valuable tools in the clinical approach of the patient with Charcot-Marie-Tooth disease, in order to define a causative mutation. In patients of South American origin, the presence of GDAP1 gene mutations should be considered, especially the Q163X mutation, as the cause of CMT4A disease.