title: Histochemical examination of osteoblastic activity in op/op mice with or without injection of recombinant M-CSF.
abstract: Osteopetrotic (op/op) mice do not exhibit bone remodeling because of defective osteoclast formation caused by the depletion of macrophage colony-stimulating factor (M-CSF). In the present study, we investigated tibial bones of op/op mice with or without prior injections of M-CSF to determine whether osteoclast formation and subsequent bone resorption could activate osteoblasts, which is known as a "coupling" phenomenon. In op/op mice, no osteoclasts were present, but the metaphyseal osteoblasts adjacent to the growth plate cartilage seemed to be active, revealing an intense alkaline phosphatase (ALPase) immunoreactivity. Consequently, primary trabecular bones were extended continuously to the diaphysis, indicating that bone modeling is well achieved in op/op mice. In contrast with the metaphysis, most of the diaphyseal osteoblasts were flattened and showed weak ALPase activity, and, as a result, they seemed to be less active. Osteopontin (OPN) was localized slightly at the interface between bone and cartilage matrices of the primary trabeculae. In contrast, in op/op mice injected with M-CSF, tartrate-resistant acid phosphatase-positive osteoclasts appeared, resorbing trabecular bones of the diaphyseal region. The diaphyseal osteoblasts in the vicinity of the active osteoclasts were cuboidal and exhibited strong ALPase immunoreactivity. OPN was observed not only at the bone-cartilage interface, but also significantly on the resorption lacunae beneath the bone-resorbing osteoclasts. These observations indicate that the activation of diaphyseal osteoblasts appears to be coupled with osteoclast formation and subsequent osteoclastic bone resorption. Alternatively, the metaphyseal osteoblasts at the chondro-osseous junction seemed to be less affected by osteoclastic activity.
authors.affiliation: Department of Physical Therapy, School of Health Science, Niigata University of Health and Welfare, Niigata, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Nishino
authors.forename: N
authors.initials: N
authors.lastname: Amizuka
authors.forename: H
authors.initials: H
authors.lastname: Ozawa
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D007267:Injections; D007527:Isoenzymes / Q000378:metabolism; D016173:Macrophage Colony-Stimulating Factor / Q000494:pharmacology*; D051379:Mice; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D010006:Osteoblasts / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010022:Osteopetrosis / Q000188:drug therapy / Q000235:genetics / Q000473:pathology*; D053495:Osteopontin; D011994:Recombinant Proteins / Q000494:pharmacology; D012795:Sialoglycoproteins / Q000378:metabolism; D000071681:Tartrate-Resistant Acid Phosphatase; D013977:Tibia / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure
chemical_list: D007527:Isoenzymes; D011994:Recombinant Proteins; D012795:Sialoglycoproteins; C506896:Spp1 protein, mouse; D053495:Osteopontin; D016173:Macrophage Colony-Stimulating Factor; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase