Evaluation of the biocompatibility of experimentally manufactured portland cement: an animal study

Objectives: The purpose of this study was to evaluate the biocompatibility of MTA and the experimentally manufactured portland cement (EMPC). Study design: Twenty one Sprague Dawley (SD) rats were allocated to testing of three groups. Group I and Group II included ProRoot MTA and the EMPC. The materials were mixed with distilled water and placed in polyethylene tubes. The tubes were implanted subcutaneously in the dorsal region of the animals. Group III served as control; the implanted polyethylene tubes remained empty. At 7, 14, and 28 days after the implantation, the animals were sacrificed and the implants were removed with the surrounding tissues. The specimens were prepared for histological examination to evaluate the inflammatory response. Results: No significant difference was found between tissue reactions against the tested materials (p>0.05). Also, control group showed similar results(p>0.05). Conclusions: Results suggest that the EMPC has the potential to be used in clinical conditions in which ProRoot MTA is indicated. MTA and the EMPC show comparable biocompatibility when evaluated in vivo. Although the results are supportive for the EMPC, more studies are required before the safe clinical use of the EMPC

Case Report Induction Of Maturogenesis by Partial Pulpotomy: 1 Year Follow-Up

In cariously exposed immature permanent teeth, the treatment choice is controversial in pediatric dentistry. Radical root canal treatment usually appears to be the solution for these teeth. Even partial pulpotomy is a vital treatment for traumatically exposed immature permanent teeth; extending the borders of indication towards cariously exposed immature permanent teeth with reversible pulpitis may abolish the necessity of pulpectomy. This article describes the partial pulpotomy of a cariously affected immature permanent teeth and the follow-up for 1 year. A healthy 11-year-old male patient was referred to Gazi University Faculty of Dentistry Department of Pediatric Dentistry. The patient had reversible pulpitis symptoms on teeth numbered 45. At radiographic examination, immature apex and deep caries lesion were observed and partial pulpotomy was performed by using calcium hydroxide to maintain vitality of the pulp and allow continued development of root dentin expecting the root will attain full maturity. Clinical and radiographic follow-up demonstrated a vital pulp besides not only closure of the apex (apexogenesis), but also physiologic root development (maturogenesis) after 1 year. Partial pulpotomy is an optional treatment for cariously exposed immature permanent teeth for preserving vitality and physiological root development

Establishing the phenotypic spectrum of ZTTK syndrome by analysis of 52 individuals with variants in SON

Zhu–Tokita–Takenouchi–Kim (ZTTK) syndrome, an intellectual disability syndrome first described in 2016, is caused by heterozygous loss-of-function variants in SON. Its encoded protein promotes pre-mRNA splicing of many genes essential for development. Whereas individual phenotypic traits have previously been linked to erroneous splicing of SON target genes, the phenotypic spectrum and the pathogenicity of missense variants have not been further evaluated. We present the phenotypic abnormalities in 52 individuals, including 17 individuals who have not been reported before. In total, loss-of-function variants were detected in 49 individuals (de novo in 47, inheritance unknown in 2), and in 3, a missense variant was observed (2 de novo, 1 inheritance unknown). Phenotypic abnormalities, systematically collected and analyzed in Human Phenotype Ontology, were found in all organ systems. Significant inter-individual phenotypic variability was observed, even in individuals with the same recurrent variant (n = 13). SON haploinsufficiency was previously shown to lead to downregulation of downstream genes, contributing to specific phenotypic features. Similar functional analysis for one missense variant, however, suggests a different mechanism than for heterozygous loss-of-function. Although small in numbers and while pathogenicity of these variants is not certain, these data allow for speculation whether de novo missense variants cause ZTTK syndrome via another mechanism, or a separate overlapping syndrome. In conclusion, heterozygous loss-of-function variants in SON define a recognizable syndrome, ZTTK, associated with a broad, severe phenotypic spectrum, characterized by a large inter-individual variability. These observations provide essential information for affected individuals, parents, and healthcare professionals to ensure appropriate clinical management