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OBJECTIVES: This study evaluated surface roughness, biaxial flexural strength, and phase transformation of 5Y-PSZ after grinding and polishing with different protocols. MATERIAL AND METHODS: Two commercial 5Y-PSZ, Lava Esthetic (L) and Cercon xt (C), were used and divided into 3 groups: LC and CC represented unpolished control groups; LE and CE were polished with protocol I (EVE DIASYNT® PLUS HP following with EVE DIACERA RA); and LJ and CJ were polished with protocol II (Superfine diamond bur following with Jota ZIR Gloss polishing kit). Surface roughness was evaluated after polishing step-by-step with a contact-type profilometer. After high-gross polishing, the specimens were subjected to biaxial flexural strength test, crystallographic microstructure analysis using an X-ray diffractometer (XRD), and surface micro-topography using scanning electron microscopy (SEM). STATISTICAL ANALYSIS: Surface roughness differences after each step and biaxial flexural strength between groups were evaluated with one-way ANOVA, followed by Bonferroni post-hoc analysis. Changes in surface roughness across four different time points within groups were assessed using one-way repeated measures ANOVA, followed by Bonferroni post-hoc analysis. RESULTS: After high-gross polishing, both polishing protocols showed significantly lower surface roughness than the grinding group (p < 0.05). The LE and CE groups exhibited the highest surface roughness values, which were significant differences from the LJ and CJ groups (p < 0.05). The LE group showed significantly lower biaxial flexural strength compared to the LC group (p < 0.05). However, there was no statistically significant difference in the CE and CJ groups compared to the control group (p > 0.05). Furthermore, all polishing protocols did not change the phase transformation of zirconia. CONCLUSION: Polishing protocol II provided a smoother surface than the protocol I after high-gross polishing, while the biaxial flexural strength of materials remained unaffected.
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OBJECTIVES: To identify etiologic variants and perform deep dental phenotyping in patients with amelogenesis imperfecta (AI). METHODS: Three patients of two unrelated families were evaluated. Genetic variants were investigated by exome and Sanger sequencing. An unerupted permanent third molar (AI1) from Patient1 and a deciduous first molar (AI2) from Patient2, along with three tooth-type matched controls for each were characterized. RESULTS: All three patients harbored biallelic pathogenic variants in FAM20A, indicating AI1G. Of the four identified variants, one, c.1231C > T p.(Arg411Trp), was novel. Patient1 possessed the largest deletion, 7531 bp, ever identified in FAM20A. In addition to hypoplastic enamel, multiple impacted teeth, intrapulpal calcification, pericoronal radiolucencies, malocclusion, and periodontal infections were found in all three patients, gingival hyperplasia in Patient1 and Patient2, and alveolar bone exostosis in Patient3. Surface roughness was increased in AI1 but decreased in AI2. Decreased enamel mineral density, hardness, and elastic modulus were observed in AI1 enamel and dentin and AI2 dentin, along with decreased phosphorus, increased carbon, and increased calcium/phosphorus and carbon/oxygen ratios. Severely collapsed enamel rods and disorganized dentin-enamel junction were observed. CONCLUSIONS: We report a novel FAM20A variant and, for the first time, the defective mineral composition and physical/mechanical properties of AI1G teeth.
Assuntos
Amelogênese Imperfeita , Proteínas do Esmalte Dentário , Humanos , Amelogênese Imperfeita/genética , Amelogênese Imperfeita/patologia , Mutação , Proteínas do Esmalte Dentário/genética , Fósforo , Minerais , CarbonoRESUMO
OBJECTIVE: This study aimed to develop enamel substitute material using a mechanochemical technique. MATERIALS AND METHODS: Hydroxyapatite was synthesized with and without tricalcium phosphate under uniaxial pressing of 10 and 17 MPa (HA10, HA17, BCP10, and BCP17), followed by sintering at 1250 °C for 2 h. Human enamel and dentin blocks were used as control groups. The mechanical properties were determined by compressive strength test and Vickers microhardness. The data were analyzed with one-way ANOVA and LSD post-hoc test (α = 0.05). The phase formation and morphology of the specimens were characterized by X-ray diffraction (XRD) and scanning electron microscopy (SEM). RESULTS: HA17 and HA10 had compressive strength values comparable to enamel and dentin, respectively (p > 0.05). The microhardness of all synthesized groups was significantly higher than that of tooth structures (p < 0.05). From the XRD graphs, only the hydroxyapatite peak was observed in the control and HA groups. SEM images showed homogeneous hydroxyapatite grains in all groups, while the BCP groups contained higher porosities. CONCLUSIONS: Both HA10 and HA17 are suitable for use as the inorganic part of dentin and enamel substitutes.
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OBJECTIVES: To characterize phenotype and genotype of amelogenesis imperfecta (AI) in a Thai patient, and review of literature. MATERIALS AND METHODS: Variants were identified using trio-exome and Sanger sequencing. The ITGB6 protein level in patient's gingival cells was measured. The patient's deciduous first molar was investigated for surface roughness, mineral density, microhardness, mineral composition, and ultrastructure. RESULTS: The patient exhibited hypoplastic-hypomineralized AI, taurodontism, and periodontal inflammation. Exome sequencing identified the novel compound heterozygous ITGB6 mutation, a nonsense c.625 G > T, p.(Gly209*) inherited from mother and a splicing c.1661-3 C > G from father, indicating AI type IH. The ITGB6 level in patient cells was significantly reduced, compared with controls. Analyses of a patient's tooth showed a significant increase in roughness while mineral density of enamel and microhardness of enamel and dentin were significantly reduced. In dentin, carbon was significantly decreased while calcium, phosphorus, and oxygen levels were significantly increased. Severely collapsed enamel rods and a gap in dentinoenamel junction were observed. Of six affected families and eight ITGB6 variants that have been reported, our patient was the only one with taurodontism. CONCLUSION: We report the hypoplasia/hypomineralization/taurodontism AI patient with disturbed tooth characteristics associated with the novel ITGB6 variants and reduced ITGB6 expression, expanding genotype, phenotype, and understanding of autosomal recessive AI.
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OBJECTIVE: Dentinogenesis imperfecta (DI) requires dental treatment. This study investigated the characteristics of DI teeth associated with osteogenesis imperfecta (OI) and COL1A2 mutations. STUDY DESIGN: Whole exome and Sanger sequencing were performed. Three primary teeth (called "OIDI teeth") obtained from 3 unrelated COL1A2 patients were investigated and compared with 9 control teeth from age-matched healthy individuals using colorimetry, micro-computed tomography, Knoop microhardness, energy dispersive X-ray spectroscopy, scanning electron microscopy, and histology. RESULTS: All patients were identified with heterozygous glycine substitutions in COL1A2. The COL1A2 mutations, c.1531G>T and c.2027G>T, were de novo, whereas c.3106G>C was inherited. OIDI1, 2, and 3 teeth had a substantial decrease in dentin microhardness and lightness. OIDI2 enamel microhardness was significantly reduced, whereas OIDI1 and 3 had enamel microhardness comparable to that of control individuals. The OIDI1 pulp cavity was large; OIDI2 was narrow; and OIDI3 was obliterated. OIDI1 and 3 had significantly higher carbon levels than those in control individuals. Numerous ectopic calcified masses, sparse and obstructed dentinal tubules, dentin holes, and collagen disorientation were observed. CONCLUSIONS: OIDI teeth had reduced lightness and variable pulp morphology. Weak dentin, mineral disproportion, and abnormal ultrastructure could contribute to the brittleness of OIDI teeth and adhesive restoration failure. Here, we expand the phenotypic spectrum of COL1A2 mutations and raise awareness among dentists seeing patients with OI.
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Dentinogênese Imperfeita , Osteogênese Imperfeita , Colágeno Tipo I/genética , Dentina , Dentinogênese Imperfeita/genética , Humanos , Mutação , Osteogênese Imperfeita/diagnóstico por imagem , Osteogênese Imperfeita/genética , Microtomografia por Raio-XRESUMO
OBJECTIVES: To investigate tooth ultrastructure and mutation of two patients in a family affected with osteogenesis imperfecta (OI) type IV and dentinogenesis imperfecta (DGI). METHODS: Mutations were detected by whole exome and Sanger sequencing. The permanent second molar obtained from the proband (DGI1) and the primary first molar from his affected son (DGI2) were studied for their color, roughness, mineral density, hardness, elastic modulus, mineral content, and ultrastructure, compared to the controls. RESULTS: Two novel missense COL1A2 variants, c.752C > T (p.Ser251Phe) and c.758G > T (p.Gly253Val), were identified in both patients. The c.758G > T was predicted to be the causative mutation. Pulp cavities of DGI1 (permanent teeth) were obliterated while those of DGI2 (primary teeth) were wide. The patients' teeth had darker and redder colors; reduced dentin hardness; decreased, disorganized, and scattered dentinal tubules and collagen fibers; and irregular dentinoenamel junction (DEJ), compared to controls. Lacunae-like structures were present in DGI2. CONCLUSIONS: We reported the novel causative mutation, c.758G > T (p.Gly253Val), in COL1A2 for OI type IV and DGI. The DGI dentin demonstrated inferior mechanical property and ultrastructure, suggesting severe disturbances of dentin formation. These could contribute to fragility and prone to infection of DGI teeth. This study expands phenotypic and genotypic spectra of COL1A2 mutations.