Orthodontic management of severe inversely impacted maxillary central incisors: a case series.

Background: Abnormal positioning and dislocation of the central incisor can disturb tooth eruption. Generally, inversely impacted maxillary central incisors do not erupt naturally. Performing traction and applied extrusion of an inversely impacted maxillary central incisor with a high inclination angle of the crown is challenging.

GSK3beta inhibitor-induced dental mesenchymal stem cells regulate ameloblast differentiation.

Objectives: Epithelial-mesenchymal interactions are extremely important in tooth development and essential for ameloblast differentiation, especially during tooth formation. We aimed to identify the type of mesenchymal cells important in ameloblast differentiation.

Methods: We used two types of cell culture systems with chambers and found that a subset of debtal mesenchimal cells is important for the differentiatiuon of dental spithelial cells into ameloblasts.

The Retention Effect of Resin-Based Desensitizing Agents on Hypersensitivity-A Randomized Controlled Trial.

Recently, the development of dental materials has increased the availability of various hyperesthesia desensitizers. However, there are no studies on the duration of retreatment in terms of adherence rates. Thus, the adhesion rates of resin-based desensitizers were investigated.

Evaluation of a Hypersensitivity Inhibitor Containing a Novel Monomer That Induces Remineralization-A Case Series in Pediatric Patients.

Background: Recently, tooth deformities have been frequently encountered by pediatric dentists. Severe enamel hypomineralization sometimes induces pain such as hyperesthesia, but composite resin restoration is difficult because it often detaches without any cavity preparation. Resin-based hypersensitivity inhibitors for tooth physically seal the dentinal tubules.

Connexin 43-Mediated Gap Junction Communication Regulates Ameloblast Differentiation ERK1/2 Phosphorylation.

Connexin 43 (Cx43) is an integral membrane protein that forms gap junction channels. These channels mediate intercellular transport and intracellular signaling to regulate organogenesis. The human disease oculodentodigital dysplasia (ODDD) is caused by mutations in Cx43 and is characterized by skeletal, ocular, and dental abnormalities including amelogenesis imperfecta.

Connexin 43 Is Necessary for Salivary Gland Branching Morphogenesis and FGF10-induced ERK1/2 Phosphorylation.

Cell-cell interaction via the gap junction regulates cell growth and differentiation, leading to formation of organs of appropriate size and quality. To determine the role of connexin43 in salivary gland development, we analyzed its expression in developing submandibular glands (SMGs). Connexin43 (Cx43) was found to be expressed in salivary gland epithelium.

The enzyme engineering of mutant homodimer and heterodimer of coproporphyinogen oxidase contributes to new insight into hereditary coproporphyria and harderoporphyria.

Hereditary coproporphyria (HCP) is an autosomal dominant-inherited disease of haem biosynthesis caused by partial deficiency of the enzyme coproporphyrinogen oxidase (CPOX). Patients with HCP show <50% of normal activity and those with the rare autosomal recessive harderoporphyria accumulate harderoporphyrinogen, an intermediate porphyrin of the CPOX reaction. To clarify the relationship of the low enzyme activity with these diseases, we expressed mutant CPOX carrying His-tag from these porphyria patients and co-expressed mutant CPOX carrying His-tag and normal CPOX carrying HA-tag in a tandem fashion in Escherichia coli.