The objective of regenerative medicine is to allow cells to induce the regeneration of body tissues, resulting in therapeutic repair of detective tissues as well as substitution of the biological functions of damaged organs. With the development of research in basic medical science and biology on cells, it is indispensable to create a suitable environment for the cells to induce regeneration in order to achieve successful tissue regeneration. Tissue engineering is the biomedical technology or methodology to build this environment, utilizing cells, the cell scaffold, growth factors, or appropriate combinations of the three. A 3-dimensional scaffold is used to assist cell proliferation and differentiation. Growth factor is often required to promote tissue regeneration, while it can induce angiogenesis necessary for the supply of oxygen and nutrients to ensure survival of the transplanted cells and to maintain the biological functions. However, growth factor used in solution form cannot always be expected to manifest biological effects because of its poor in vivo stability, unless the technology of drug delivery systems (DDS) is applied. In this paper, in addition to a brief overview of tissue engineering, several research data on tissue regeneration are presented to emphasize the significance of tissue engineering in regenerative medicine.

抄録全体を表示

Aluminum (Al) has, until recently, existed predominantly in forms that are not available to humans. Acid rain, however, has dramatically increased the amount of Al in biological ecosystems, resulting in the well-documented destructive effects in fish and plant species¹⁾. Although the occurrence of dialysis osteomalacia is closely associated with long-term Al accumulation, the exact role of this metal in the pathogenesis is not yet known. The effects of Al on healthy humans are, almost without exception, unknown. This ignorance has stimulated the search for animal models to obtain insight into the pathogenesis and biochemical mechanisms underlying the human disorders. In this review, several pathophysiologic mechanisms of Al toxicity in bone are summarized.

抄録全体を表示

The repair of dentin is thought to be maintained through differentiation of undefined precursor cells within the dental pulp to odontoblasts. To investigate the characteristics of these undefined precursor cells in dental pulp, mixed pulp cells and cloned cells were obtained from H-2K^b-ts A58 heterozygous transgenic mice. Differentiation of dental pulp precursor cells in vitro was assayed by RT-PCR analysis of gene expression of osteopontin, osteocalcin and dentin sialophosphoprotein (DSPP), and by von Kossa staining for mineralization. All assays were conducted on cultured mixed pulp cells and clonal cells PC1, PC8 and PC14. The results suggested that dental pulp cells could differentiate to odontoblasts in vitro. To test for chondrogenic potential, mixed pulp cells and clonal cells PC1, PC8 and PC14 were maintained in high density pellet cultures, and PC1 cells were stained with toluidine blue for glycosaminoglycans (GAG) content. To confirm the chondrocyte phenotype, the extracellular matrix of PC1 cells in pellet culture was stained with anti-type II collagen antibody. This study is the first to demonstrate that dental pulp stem cells present in the dental pulp have multi-potential to differentiate to both odontoblast and chondroblast.

抄録全体を表示

Although the craniofacial and the appendicular bones develop embryologically from different origins and show different architectures and functions, it is still unclear if there exist site-specific genetic and phenotypic differences in these bones. The aim of this study was to analyze the gene expression levels of collagen-binding small leucine-rich proteoglycans (SLRPs) and type I collagen (COLI), the major matrix proteins in bone, in mouse mandibular and femoral bone marrows. Histomorphometrical and real-time PCR analyses were performed on the two bones of two senescence-accelerated mouse (SAM) strains. SAMP8 and SAMR1, with potentially different bone phenotypes. In both mice, the trabecular bone volume was 10 times higher at the mandibular neck than at the femoral distal metaphysis. The volume in the femur but not in the mandible was slightly higher in SAMR1 than in SAMP8. The mRNAs of COLI and collagen-binding SLRPs, except decorin, were higher in the mandibular bone marrow than in the femoral marrow. Although the femoral marrow did not express fibromodulin and lumican in both mouse strains and biglycan in the SAMR1 strain, they were highly expressed in the mandibular marrow. High gene expression of these molecules in the mandibular bone may imply active bone formation and remodeling in this bone tissue.

抄録全体を表示