Morphological assessment of bone mineralization in tibial metaphyses of ascorbic acid-deficient ODS rats

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Author(s)

    • Hasegawa Tomoka
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Inoue Kiichiro
    • Department of Oral Functional Anatomy, Hokkaido University, Sapporo, Japan
    • Yamamoto Tsuneyuki
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Oohata Noboru
    • Department of Oral Rehabilitation, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Japan
    • Oda Kimimitsu
    • Division of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
    • Amizuka Norio
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Li Minqi
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Hara Kuniko
    • Pharmacological Evaluation Section, Eisai Co., Ltd., Tokyo, Japan
    • Sasaki Muneteru
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Tabata Chihiro
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Hongo Hiromi
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan
    • Suzuki Reiko
    • Department of 1 Developmental Biology of Hard Tissue, Hokkaido University, Sapporo, Japan

Abstract

Osteogenic disorder shionogi (ODS) rats carry a hereditary defect in ascorbic acid synthesis, mimicking human scurvy when fed with an ascorbic acid-deficient (<I>aa-def</I>) diet. As <I>aa-def</I> ODS rats were shown to feature disordered bone formation, we have examined the bone mineralization in this rat model. A fibrous tissue layer surrounding the trabeculae of tibial metaphyses was found in <I>aa-def</I> ODS rats, and this layer showed intense alkaline phosphatase activity and proliferating cell nuclear antigen-immunopositivity. Many osteoblasts detached from the bone surfaces and were characterized by round-shaped rough endoplasmic reticulum (rER), suggesting accumulation of malformed collagen inside the rER. Accordingly, fine, fragile fibrillar collagenous structures without evident striation were found in <I>aa-def</I> bones, which may result from misassembling of the triple helices of collagenous α-chains. Despite a marked reduction in bone formation, ascorbic acid deprivation seemed to have no effect on mineralization: while reduced in number, normal matrix vesicles and mineralized nodules could be seen in <I>aa-def</I> bones. Fine needle-like mineral crystals extended from these mineralized nodules, and were apparently bound to collagenous fibrillar structures. In summary, collagen mineralization seems unaffected by ascorbic acid deficiency in spite of the fine, fragile collagenous fibrils identified in the bones of our animal model.

Journal

  • Biomedical Research

    Biomedical Research 32(4), 259-269, 2011

    Biomedical Research Press

Codes

  • NII Article ID (NAID)
    130004903823
  • NII NACSIS-CAT ID (NCID)
    AA00110128
  • Text Lang
    ENG
  • Article Type
    journal article
  • ISSN
    0388-6107
  • Data Source
    IR  J-STAGE 
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