KMT2d regulates tooth enamel development.

Amelogenesis, the process of enamel formation, is tightly regulated and essential for producing the tooth enamel that protects teeth from decay and wear. Disruptions in amelogenesis can result in amelogenesis imperfecta, a group of genetic conditions characterized by defective enamel, including enamel hypoplasia, marked by thin or underdeveloped enamel. Mutations in the KMT2D (MLL4) gene, which encodes a histone H3-lysine 4-methyltransferase, are associated with Kabuki syndrome, a developmental disorder that can involve dental anomalies such as enamel hypoplasia.

MLL4 regulates postnatal palate growth and midpalatal suture development.

MLL4, also known as KMT2D, is a histone methyltransferase that acts as an important epigenetic regulator in various organogenesis programs. Mutations in the gene are the major cause of Kabuki syndrome, a human developmental disorder that involves craniofacial birth defects, including anomalies in the palate. This study aimed to investigate the role of MLL4 and the underlying mechanisms in the development and growth of the palate.

Innovative digital tools for new trends in teaching and assessment methods in medical and dental education.

With the goal of providing optimal care to patients, student-centered active learning and the development of clinical competency have become vital components of the education of future physicians capable of sustainably coping with future challenges. However, the shape of future medicine is dramatically changing based on advances in information and communication technology, and the current classroom model seems to have difficulties in fully preparing students for the future of medicine. New trends in teaching and assessment methods include computer-aided instruction, virtual patients, augmented reality, human patient simulations, and virtual reality for the assessment of students’ competency.

Bmp4-Msx1 signaling and Osr2 control tooth organogenesis through antagonistic regulation of secreted Wnt antagonists.

Mutations in MSX1 cause craniofacial developmental defects, including tooth agenesis, in humans and mice. Previous studies suggest that Msx1 activates Bmp4 expression in the developing tooth mesenchyme to drive early tooth organogenesis. Whereas Msx1 mice exhibit developmental arrest of all tooth germs at the bud stage, mice with neural crest-specific inactivation of Bmp4 (Bmp4), which lack Bmp4 expression in the developing tooth mesenchyme, showed developmental arrest of only mandibular molars.

Hippo pathway/Yap regulates primary enamel knot and dental cusp patterning in tooth morphogenesis.

The shape of an individual tooth crown is primarily determined by the number and arrangement of its cusps, i.e., cusp patterning.