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Takeyasu Maeda

Publications and source records attributed to Takeyasu Maeda.

49 records · Page 3Linked to original sources

Regeneration of nerve fibres in the peri-implant epithelium incident to implantation in the rat maxilla as demonstrated by immunocytochemistry for protein gene product 9.5 (PGP9.5) and calcitonin gene-related peptide (CGRP).

The response of nerve fibres in the peri-implant epithelium to titanium implantation was investigated with an experimental model using rat maxilla and immunohistochemical techniques. The latter employed antibodies to protein gene product 9.5 (PGP9.5), and to calcitonin gene-related peptide (CGRP). In control rats without an implantation, a dense innervation of PGP9.5- and CGRP-positive nerve fibres was recognized throughout the junctional epithelium, as has been previously reported. A titanium-implantation induced a remarkable inflammatory reaction, as well as the destruction of covering epithelial cells. By 3-5 days post-implantation, inflammatory reaction showed a tendency to disappear, and the peri-implant epithelium showed proliferation and down-growth along the implant. At this stage, no nerve fibres were found around the peri-implant epithelium. At 10 days, a few nerve fibres reached the basal cell layers of the peri-implant epithelium, and entered it 15 days after implantation when the peri-implant epithelial cells showed morphological features roughly resembling those of normal junctional epithelial cells. At the complete osseointegration stage (days 20-30), the PGP9.5- and CGRP-positive nerve fibres, thin and beaded in appearance, were found distributed in the peri-implant epithelium. After 20 days, the numerical density of the intraepithelial nerves in the peri-implant epithelium appeared the same as, or less than, that in the normal junctional epithelium. These findings indicate that the peri-implant epithelium shows the same innervation as that in normal junctional epithelium, and that the intraepithelial nerve fibres in the peri-implant epithelium might have diverse functions, which have been suggested in the literature.

Animals↗

Different distribution of immunocompetent cells in the dentogingival junction during root formation in rat molars.

The distribution of immunocompetent cells in the dentogingival junction of rat molars during root formation was investigated by immunocytochemistry using antibodies to class II major histocompatibility complex (MHC) molecules (OX6-antibody) and monocyte/macrophage lineage cells (ED1-antibody) as well as by histochemical reaction for periodic acid-Schiff (PAS). Two portions (the junctional epithelium in the mesial gingiva of the first molar, and the interdental gingiva between the first and second molars) were selected for observations. At the eruption stage of the first molar (16-18 days after birth), OX6-positive cells, dendritic or oval in shape, were abundantly distributed in the connective tissue between the oral epithelium and tooth germ. Positive cells with slender cell processes were also found beneath the ameloblast layer. At the commencement stage of the first molar occlusion (24-28 days after birth), numerous OX6-positive cells displaying a dendritic fashion existed preferentially in the mesial gingiva, but were fewer in the interdental gingiva. In contrast, the interdental gingiva showed a denser distribution of ED1-positive cells and PAS-reactive polymorphonuclear leukocytes (PMLs) than the mesial gingiva. At the completion stage of root formation (100-120 days after birth), the OX6-immunopositive cells invaded the deeper position of the mesial gingiva with the downgrowth of the epithelium; they had a considerably higher cell density compared with those in the interdental gingiva where PAS-reactive PMLs persisted. These findings indicated that the immunocompetent cells showed a region-specific distribution and cell density by their roles in immune response.

Ameloblasts↗

Tissue response to titanium implantation in the rat maxilla, with special reference to the effects of surface conditions on bone formation.

Tissue responses to titanium implantation with two different surface conditions in our established implantation model in rat maxillae were investigated by light and transmission electron microscopy and by histochemistry for tartrate-resistant acid phosphatase (TRAPase) activity. Here we used two types of implants with different surface qualities: titanium implants sandblasted with Al2O3 (SA-group) and implants coated with hydroxyapatite (HA-group). In both groups, bone formation had begun by 5 days postimplantation when the inflammatory reaction had almost disappeared in the prepared bone cavity. In the SA-group, however, the bone formation process in the bone cavity was almost identical to that shown in our previous report using smooth surfaced implants (Futami et al. 2000): new bone formation, which occurred from the pre-existing bone toward the implant, was preceded by active bone resorption in the lateral area with a narrow gap, but not so in the base area with a wide gap. In the HA-group, direct bone formation from the implant toward the pre-existing bone was recognizable in both lateral and base areas. Many TRAPase-reactive cells were found near the implant surface. On the pre-existing bone, new bone formation occurred with bone resorption by typical osteoclasts. Osseointegration around the implants was achieved by postoperative day 28 in both SA- and HA-groups except for the lateral area, where the implant had been installed close to the cavity margin. These findings indicate that ossification around the titanium implants progresses in different patterns, probably dependent on surface properties and quality.

Acid Phosphatase↗

Defective bone remodelling in osteoprotegerin-deficient mice.

Previous studies have reported enhanced osteoclastogenesis, increased bone resorption and osteoporosis in osteoprotegerin (OPG)-deficient mice. In the present study, we show that the tibial epiphyses contain abundant, thin trabeculae lined with numerous osteoclasts and cuboidal osteoblasts. The increase in osteoblasts and osteoclasts was associated with a dramatic increase in calcein labelling of the mineralization fronts and replacement of much of the intertrabecular marrow with numerous alkaline phosphatase-positive preosteoblasts. Furthermore, the discrete, linear cement lines seen in wild-type mice were replaced by a randomly oriented meshwork of cement lines that were stained intensely for tartrate-resistant acid phosphatase and osteopontin in the OPG-/- mice. These indices of accelerated bone remodelling in mutant bone were associated with irregular trabecular surfaces, a disorganized collagen matrix interspersed with amorphous ground substance and numerous fissures between old and new bone. In total, these observations indicate that enhanced osteoclastic activity in OPG-/- epiphyses led to a coupled increase in osteoblast differentiation and activity and an increase in bone remodelling. The high bone turnover, disorganized matrix and impaired attachment of new to old bone in the cement lines in OPG-/- mice appear to cause bone fragility.

Animals↗

The involvement of brain-derived neurotrophic factor (BDNF) in the regeneration of periodontal Ruffini endings following transection of the inferior alveolar nerve.

The present study employed immunohistochemistry for protein gene product 9.5 (PGP 9.5) to examine the regeneration process of Ruffini endings, the primary mechanoreceptor in the periodontal ligament, in heterozygous mice with targeted disruption of the brain-derived neurotrophic factor (BDNF) gene and their littermates, following transection of the inferior alveolar nerve. When immunostained for PGP 9.5, periodontal Ruffini endings appeared densely distributed in the periodontal ligament of the heterozygous mice, but the density of the positively stained nerve fibers in the ligament was 20% lower than that in the control littermates. At 3 days after surgery, the PGP 9.5-positive neural elements had disappeared; they began to appear in the periodontal ligament of both animals at 7 days. However, the recovery pattern of the PGP 9.5-positive nerves differed between heterozygous and wild type mice, typical periodontal Ruffini endings morphologically identical to those in the control group appeared in the wild-type mice at 7 days, whereas such Ruffini endings were detectable in the heterozygous mice at 28 days, though much smaller in number. On day 28, when PGP 9.5-positive nerves were largely regenerated in wild type mice, their distribution was much less dense in the ligament of the heterozygous mice than in the non-treated heterozygous mice. The density of PGP 9.5-positive nerve fibers was significantly lower in the heterozygous mice than in wild type mice at any stage examined. These data showing that a reduced expression of BDNF causes delayed regeneration of the periodontal Ruffini endings suggest the involvement of BDNF in the regeneration process of these mechanoreceptors.

Animals↗

Synovial membrane in the temporomandibular joint--its morphology, function and development.

This paper reviews recent findings of the synovial membrane, in particular the morphology, function and development of synovial lining cells, in the temporomandibular joint (TMJ). Electron microscopic studies have confirmed the synovial membrane in TMJ consists of macrophage-like type A cells and fibroblast-like type B cells identical to those in other systematic joints. The macrophage-like type A cells react with anti-macrophage and macrophage-derived substances including the major histocompatibility class II molecule, and show a drastic increase in their number in the inflamed synovial membrane. In addition, they have the ability to produce substances involved in the progression of TMJ inflammation such as nitric oxide and inducible nitric oxide synthase. Observation of osteopetrotic mice revealed that macrophage-like type A cells in TMJ are derived from monocyte lineage. Immunocytochemistry for 25kDa heat shock protein was able to depict the entire shape of fibroblast-like type B cells including their unique processes. The expression of an estrogen receptor alpha-immunoreaction in the fibroblast-like type B cells may explain the etiology of temporomandibular disorders at a higher frequency in females than in males, suggesting that TMJ is a target tissue for estrogen. Furthermore, fibroblast-like type B cells are equipped with a basement membrane to serve as an adhesion molecule for the fibroblast-like type B cells to keep their epithelial arrangement. A clear understanding of the morphology of the intact synovial membrane will serve to clarify the etiology and development of temporomandibular disorders.

Animals↗

The periodontal Ruffini endings in brain derived neurotrophic factor (BDNF) deficient mice.

Innervation and terminal morphology in the lingual periodontal ligament of the incisor were investigated in brain derived neurotrophic factor (BDNF) heterozygous mice and littermate wild-type mice (aged two months) using immunohistochemistry for protein gene product 9.5 (PGP 9.5), a general neuronal marker. In addition, computer-assisted quantitative analysis was performed for a comparison of neuronal density in the periodontal ligament between heterozygous and wild-type mice. In wild-type mice, the periodontal ligament was found to be richly innervated by the mechanoreceptive Ruffini endings and nociceptive free nerve endings in the alveolus-related part of the periodontal ligament. The periodontal Ruffini endings in the wild-type mice incisor ligament were classified into two types: type I with ruffled outlines, and type II with a smooth outline. BDNF heterozygous mice showed malformations of the type I Ruffini endings which included fewer nerve fibers and fewer ramifications than those in wild-type mice as well as smooth outlines of the axon terminals. Quantitative analysis under a confocal microscope showed a roughly 18% reduction in neuronal density in the periodontal ligament of the heterozygous mice. These findings suggest that the development and maturation of the periodontal Ruffini endings require BDNF.

Animals↗

[Mineralization and vascular invasion during endochondral bone formation].

The epiphyseal cartilage is composed of the distinct zones of resting, proliferative and hypertrophic chondrocytes. The intercolumnar cartilage matrix of the hypertrophic zone is subjected to mineralization whereas the transverse partitions of the cartilage column are poorly mineralized. Therefore, mineralized cartilage matrices are formed parallel to the longitudinal axis of the epiphyseal cartilage. Vascular endothelial cells invade the cartilage by penetrating the poorly mineralized transverse partition at the chondro-osseous junction, resulting in the exposure of mineralized intercolumnar matrix to bony tissue. The exposed mineralized cartilage matrices appear to serve as scaffolds for osteoblastic attachment. These osteoblasts deposit bone matrices onto the cartilage cores, forming primary trabecular bones. Vascular endothelial growth factor, VEGF, is a strong angiogenic factor, and play a pivotal role in vascular invasion into cartilage. The invading endothelial cells possess the receptor for VEGF, and secret matrix metallo protatenase to digest the cartilage matrices of the unmineralized transverse partition of the column.

English Abstract↗

Expression of galanin receptor-1 (GALR1) in the rat trigeminal ganglia and molar teeth.

The expression of galanin receptor-1 (GALR1) was investigated in the rat trigeminal ganglion by using immunocytochemistry and in situ hybridization. In addition, the regional distribution of GALR1-immunoreactive pulpal nerves and their ultrastructure were examined in the molar teeth. In the trigeminal ganglion, the immunoreactivity for GALR1 was recognizable in about 30% of the total number of neurons. Most of the cell bodies were small to medium in size. Analysis of serially cut sections alternately stained with GALR1 and galanin antisera demonstrated that some GALR1-positive cells displayed immunoreactivity for galanin. In situ hybridization analysis, expression of GALR1 mRNA was detected in trigeminal ganglion cells. The cell size distribution was similar to that of GALR1-immunoreactive cells. In the dental pulp, a small number of nerve fibers displayed immunoreactivity for GALR1. The labeled fibers formed terminal arbors in the coronal pulp around and within the odontoblast cell layer, but never penetrated into the predentin and dentin. Ultrastructurally, GALR1 immunoreactivity in the dental pulp was confined to the axoplasm of unmyelinated nerve fibers. The present study provided new evidence that unmyelinated primary afferents innervating dental pulp possessed galanin receptor, and suggests the existence of nociceptive primary afferents functioning as autocrine cells.

Animals↗

Biological action of parathyroid hormone (PTH)-related peptide (PTHrP) mediated either by the PTH/PTHrP receptor or the nucleolar translocation in chondrocytes.

Parathyroid hormone (PTH)-related peptide (PTHrP) has been believed to act by binding the common receptor to PTH (PTH/PTHrP receptor). However, PTHrP is localized not only in the secretory pathway, but also in nucleoli by virtue of its nucleolar targeting signal (NTS). This review demonstrates the bipartite action of PTHrP on chondrocytes, the receptor-mediated and -independent signaling pathway. Mice with deletion of the PTHrP gene were characterized by a chondrodysplasia due to markedly reduced proliferation of epiphyseal chondrocytes. The PTH/PTHrP receptor was localized mainly in proliferative chondrocytes in the epiphyseal cartilage, indicating that PTHrP modulates normal proliferation via the receptor. In contrast to the receptor-mediated action, the mid-region of the amino acid sequence of PTHrP contains an NTS. The PTHrP-translation was found to initiate from both methionine-coding AUG and downstream leucine-coding CUGs in its signal sequence. When translated from CUGs, PTHrP accumulated in the nucleoli, and the translation from AUG localized PTHrP in both the Golgi apparatus and nucleoli. Therefore, nucleolar PTHrP appears to be derived from the translation initiating from both AUG and CUGs. A chondrocytic cell line expressing a full-length PTHrP, but not PTHrP lacking NTS, were resistant to apoptosis caused by serum depletion, suggesting that the nucleolar PTHrP in chondrocytes serves as a survival factor against apoptosis. Thus, PTHrP regulates chondrocyte proliferation, differentiation and apoptosis by mediating its receptor or acting directly on the nucleolus.

Animals↗

Expression of heat-shock protein 25 immunoreactivity in the dental pulp and enamel organ during odontogenesis in the rat molar.

The present immunocytochemical study reports on the expression of heat-shock protein (Hsp) 25 during odontogenesis in rat molars from postnatal 1 to 100 days. Hsp 25 immunoreactivity (IR) appeared in the immature dental mesenchymal cells and the differentiating and differentiated odontoblasts. At 30 days, the coronal odontoblasts retained intense Hsp25-IR, whereas the odontoblasts in the root and floor pulp were initially weak or negative but increased in IR in the later stages, indicating that the expression of Hsp 25 reflects the differentiation status of odontoblasts. During amelogenesis, the secretory ameloblasts were Hsp 25 immunopositive and the enamel free area (EFA) cells showed intense Hsp 25-IR when they developed a ruffled border. Ruffle-ended ameloblasts (RA) also consistently showed intense Hsp 25-IR, but smooth ended ameloblasts (SA) showed weak IR. These data suggest that Hsp 25 is related to the formation and maintenance of the ruffled border of RA and EFA cells.

Aging↗

[The biological role of blood vessels during endochondral bone formation].

Endothelial cells play an important role in endochondral bone formation. In the chondro-osseous junction, endothelial cells appear to invade into cartilage by the cellular mechanism of angiogenesis evidenced by cell duplication, disappearance of basement membranes and activated migration. The endothelial cells penetrate the unmineralized transverse partition of the cartilage columns.

English Abstract↗

[Not Available].

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Journal Article↗