Biomedical subjects

Atsushi Ohazama

Publications and source records attributed to Atsushi Ohazama.

8 recordsLinked to original sources

PubMed2007

Expression of claudins in murine tooth development.

Claudins belong to a family of transmembrane proteins that were identified as components of tight junction strands. We carried out comparative in situ hybridization analysis of 11 claudin genes (claudin1 - claudin11) during murine odontogenesis from the formation of the epithelial thickening to the cytodifferentiation stage. We identify dynamic spatiotemporal expression of 9 of the 11 claudins. At the early bell stage, two claudins (claudin1 and 4) are specifically expressed in stratum intemedium, whereas only one claudin is expressed in each of the preameloblasts (claudin2) and preodontoblasts (claudin10). At the bud stage, when the first epithelial differentiation pathways are being established, localized expression of six claudins (claudin1, 3, 4, 6, 7, and 10) identify spatial specific interactions, suggesting a hitherto unobserved complexity of epithelial organization, within the early tooth primordium.

Animals↗

PubMed2006

Effects of combined treatment with porous bovine inorganic bone grafts and bilayer porcine collagen membrane on refractory one-wall intrabony defects.

The aim of this study was to investigate the effects of a combination of porous bovine inorganic bone graft (Bio-Oss) and bilayer porcine collagen membrane (Bio-Gide) on refractory one-wall intrabony defects in dogs. Bio-Oss and Bio-Gide were applied into the refractory one-wall intrabony defect. The contralateral sites were used as controls (without the application of Bio-Oss and Bio-Gide). At 24 weeks after surgery, similar pocket depths were found in both groups. However, histologic observation revealed an infiltration of inflammatory cells in the control group caused by poor gingival architecture, whereas only a few of the experimental sites showed inflammatory infiltration. In addition to the healthy gingival tissue, periodontal tissue regeneration was observed in the experimental group. The combination of Bio-Oss and Bio-Gide was an effective treatment for refractory one-wall intrabony defects in dogs.

Alveolar Bone Loss↗

PubMed2005

[The possibility of tooth regenerative therapy].

Teeth develop from the sequential and reciprocal interactions between the oral epithelium and neural crest-derived mesenchyme. Recently, it has been reported that many factors such as Msx1, Pax9, Lef1, Bmp, Fgf, Wnt, Shh and Eda play a critical role in tooth development. It is expected that the further accumulation of evidence involved in mechanisms of tooth development and stem cell biology could lead to the development of tooth regenerative therapy based on this biological evidence.

Animals↗

PubMed2004

Traf6 is essential for murine tooth cusp morphogenesis.

Ectodermal appendages such as skin, hair, teeth, and sweat glands are affected in patients with hypohidrotic (anhydrotic) ectodermal dysplasia (HED). It has been established that mutations in the tumor necrosis factor (TNF) superfamily of molecules, i.e., ectodysplasin (EDA), EDA receptor (EDAR), and EDAR-associated death domain (EDARADD; the intracellular adaptor for EDAR), are responsible for several forms of HED in humans and mice. We show here by in situ hybridisation that another TNF family (orphan) receptor, TROY (also known TAJ, TAJ-alpha, TRADE, and TNFRSF19), is strongly coexpressed with Edar in the epithelial enamel knot signalling centres that are believe to regulate cuspal morphogenesis during murine tooth development. Traf6 is known to function as an intracellular adaptor protein for Troy and examination of Traf6 mutant mice revealed abnormalities in molar teeth that are similar but more severe than those produced by mutations in Eda signalling molecules. This finding suggests that, in additional to ectodysplasin, another TNF pathway involving Troy/Traf6 is involved in molar tooth cusp formation and identifies an essential role for a Traf in tooth development. Developmental Dynamics 229:131-135, 2004.

Animals↗

PubMed2004

TNF signalling in tooth development.

Mammalian tooth development has served as an excellent model system to investigate the intricate, interactive mechanisms of patterning, morphogenesis and cytodifferentiation during organogenesis. Teeth develop from interactions between epithelium and neural crest-derived (ecto)mesenchyme that are largely mediated by ligand-receptor signalling. It is well-established that signalling molecules of the Bmp, Fgf, Wnt and Hedgehog families, are involved at multiple stages of tooth development. Recently, however, a specific role for molecules belonging to the TNF-family of ligands in tooth morphogenesis has been identified, suggesting that this pathway, acting to activate NF-kappaB, has played an important role in the development and evolution of tooth number and shape.

Animals↗

PubMed2004

A dual role for Ikk alpha in tooth development.

IKK alpha is a component of the I kappa B kinase (IKK) complex that plays a key role in the activation of NF-kappa B. In Ikk alpha mutant mice and mice expressing a transdominant negative mutant of I kappa B alpha (cI kappa B alpha Delta N), molars have abnormal cusps, indicating that Ikk alpha is involved in cusp formation through the NF-kappa B pathway. However, Ikk alpha mutant incisors also have an earlier phenotype where epithelium evaginates outward into the developing oral cavity rather than invaginating into the underlying mesenchyme. A similar evagination of epithelium was also observed in whisker development, suggesting that Ikk alpha contributes to the direction of epithelial growth during the early stages of development in many ectodermal appendages. Since cI kappa B alpha Delta N mice have normal incisor epithelial invagination, Ikk alpha's role appears to be NF-kappa B independent. Changes in Notch1, Notch2, Wnt7b, and Shh expression found in incisor epithelium of Ikk alpha mutants suggest that this NF-kappa B-independent function is mediated by Notch/Wnt/Shh signaling pathways.

Animals↗

PubMed2003

Expression of TNF-receptor-associated factor genes in murine tooth development.

Tumor necrosis factor receptor-associated factors (TRAFs) belong to a family of intracellular adaptor proteins that mediate signaling downstream of various cell surface receptors. We carried out comparative in situ hybridization analysis of five Traf genes Traf1, Traf2, Traf3, Traf4 and Traf6 during murine odontogenesis from the formation of the epithelial thickening to the early bell stage. Traf2, Traf3 and Traf6 showed weak expression in the thickened epithelium. Expression of Traf1, Traf2 and Traf6 were observed in the outer edges of the bud epithelium whereas Traf3 was strongly expressed at the tip of the bud epithelium. Expression of Traf1, Traf4 and Traf6 were detected in the dental papilla mesenchyme. Traf2 showed restricted expression in the internal enamel epithelium of the bell stage while expression of Traf1, Traf3, Traf4 and Traf6 were observed in both the internal and the external enamel epithelium. During early odontogenesis, all five genes show dynamic spatiotemporal expression patterns.

Animals↗

PubMed2002

Tooth development is independent of a Hox patterning programme.

Hox genes have a critical role in controlling the patterning processes of many tissues by imparting positional information in embryogenesis. Patterning of the pharyngeal component of the skull (the visceroskeleton) has been proposed to be influenced by this "Hox code." Recently, it has been shown that Hox genes are associated with the evolution of jaws, loss of Hox gene expression in the first branchial arch being necessary for the transition from the agnathan condition to the gnathostome condition. Teeth develop on the first branchial arch in mammals and, therefore, might be expected to be under the control of Hox genes in a manner similar to that of the cranial skeletal elements. However, we show that, unlike cartilage and bone, the development of teeth is not affected by alterations in Hoxa2 expression. Tooth development in the first arch was unaffected by overexpression of Hoxa2, whereas recombinations of second arch mesenchyme with first arch epithelium led to tooth development within a Hoxa2-positive environment. These data demonstrate that teeth develop from local interactions and that tooth formation is not under the axial patterning program specified by the Hox genes. We propose that the evolutionary development of teeth in the first branchial arch is independent of the loss of Hox expression necessary for the development of the jaw.

Animals↗