title: Reduced osteoblastic population and defective mineralization in osteopetrotic (op/op) mice.
abstract: Osteopetrotic (op/op) mice fail to exhibit bone remodeling because of a defective osteoclast formation due to a lack of macrophage colony-stimulating factor. In this study, we investigated the femora of op/op mice to clarify whether the osteoblastic population and bone mineralization are involved in osteoclasts or their bone resorption. The op/op mice extended the meshwork of trabecular bones from the chondro-osseous junction to the diaphyseal region. In the femoral metaphyses of op/op mice, intense alkaline phosphatase (ALPase)-positive osteoblasts were observed on the metaphyseal bone in close proximity to the erosion zone of the growth plates. Von Kossa's staining revealed scattered mineralized nodules and a fine meshwork of mineralized bone matrices while the wild-type littermates developed well-mineralized trabeculae parallel to the longitudinal axis. In contrast to the metaphysis, some op/op diaphyses showed flattened osteoblasts with weak ALPase-positivity, and the other diaphyses displayed bone surfaces without a covering by osteoblasts. It is likely, therefore, that the osteoblastic population and activity were lessened in the op/op diaphyses. Despite the osteopetrotic model, von Kossa's staining demonstrated patchy unmineralized areas in the op/op diaphyses, indicating that a lower population and/or the activity of osteoblasts resulted in defective mineralization in the bone. Transmission electron microscopy disclosed few osteoblasts on the diaphyseal bones, and instead, bone marrow cells and vascular endothelial cells were often attached to the unmineralized bone. Osteocytes were embedded in the unmineralized bone matrix. Thus, osteoclasts appear to be involved in the osteoblastic population and activity as well as subsequent bone mineralization.
authors.affiliation: Division of Oral Anatomy, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, 5274, 2-Bancho, Gakkoucho-Dori, Niigata 951-8514, Japan.
authors.forename: Naoko
authors.initials: N
authors.lastname: Sakagami
authors.forename: Norio
authors.initials: N
authors.lastname: Amizuka
authors.forename: Minqi
authors.initials: M
authors.lastname: Li
authors.forename: Kiichi
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Masaaki
authors.initials: M
authors.lastname: Hoshino
authors.forename: Midori
authors.initials: M
authors.lastname: Nakamura
authors.forename: Kayoko
authors.initials: K
authors.lastname: Nozawa-Inoue
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Udagawa
authors.forename: Takeyasu
authors.initials: T
authors.lastname: Maeda
mesh_terms: D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D001696:Biomechanical Phenomena; D001857:Bone Matrix / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D016723:Bone Remodeling / Q000502:physiology; D002113:Calcification, Physiologic; D003238:Connective Tissue / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D018483:Diaphyses / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D004195:Disease Models, Animal; D005269:Femur; D006132:Growth Plate / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D006253:Haversian System / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D007150:Immunohistochemistry; D051379:Mice; D008817:Mice, Mutant Strains; D046529:Microscopy, Electron, Transmission; D010006:Osteoblasts / Q000473:pathology* / Q000502:physiology / Q000648:ultrastructure; D010010:Osteoclasts / Q000473:pathology / Q000502:physiology / Q000648:ultrastructure; D010022:Osteopetrosis / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D013977:Tibia
chemical_list: D000469:Alkaline Phosphatase