Color stability and surface roughness of artificial teeth brushed with an experimental Ricinus communis toothpaste

Aim: To evaluate, in vitro, the effect of brushing with a Ricinus communis -based experimental toothpaste on color stability and surface roughness of artificial teeth. Methods: Ninety artificial teeth (maxillary central incisors) in different shades, light and dark (NatusDent Triple Pressing, Dentbras) were used. Initial color (Spectrophotometer Easyshade, VITA) and surface roughness (Rugosimeter Surfcorder SE 1700, Kosakalab) readouts were performed. After baseline measurements, samples were assigned to 10 groups (n=9) according to the artificial tooth shade and type of toothpaste used during the mechanical brushing test (Pepsodent, MAVTEC): Sorriso Dentes Brancos – SDB, Colgate Luminous White - CLW (Colgate-Palmolive), Close up White Now - CWN (Unilever), Trihydral - THL (Perland Pharmacos) and Ricinus communis - RCE (Experimental). After 29,200 cycles of brushing, corresponding to 2 years of brushing by a healthy individual, new color and roughness readouts of the specimens were performed. Data (before and after the tests) were statistically analyzed (2-way repeated measures ANOVA, Tukey, p<0.05). Results: RCE toothpaste produced the greatest color stability for dark tooth shade and the second best color stability for light tooth shade. For surface roughness alteration, there was no difference (p>0.05) for any tested toothpaste regardless of tooth shade. Conclusions: The experimental Ricinus communis toothpaste did not cause color and surface roughness alteration in the artificial teeth, and it may be considered a suitable option for denture cleaning.

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.