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At least 505 records · Page 28Linked to original sources
PubMed1980

Characterization of endosteal bone-lining cells from fatty marrow bone sites in adult beagles.

Bone-lining cells cover the majority of trabecular bone surfaces in adult long-lived mammals. The morphology, ultrastructure, and population density of bone-lining cells was investigated in several fatty marrow trabecular bone sites in adult beagles of different ages. Although there is a low population density of bone-lining cells on bone surfaces, their total numbers greatly exceed the numbers of osteoblasts and osteoclasts found on these bone surfaces. In one of the bone sites studied, there are significantly fewer bone-lining cells in very old beagles (12-16 years old) when compared to young adult beagles (1.5-3 years old), otherwise there are no differences in the cell population that could be attributed to aging. Bone-lining cells are flattened against bone surfaces and have flat or sometimes ovoid-shaped nuclei which are often located adjacent to areas in the fatty marrow where capillaries are found. When viewed in the electron microscope, bone-lining cells contain few organelles, and the attenuated cytoplasm of these cells is well extended over bone surfaces. The bone-lining cell cytoplasm does not appear to form a continuous layer over the bone surface, as numerous gaps and spaces are seen. Bone-lining cell processes are frequently joined by junctions morphologically similar to gap junctions. Between the lamina limitans of the bone matrix and the bone-lining cell, as well as between the bone-lining cell and the adjacent fat cells, there are layers of connective tissue containing collagenous fibers and other amorphous material. These findings are discussed in relation to the possible role of bone-lining cells in the regulation of mineral homeostasis.

Aging↗
PubMed2002

Biomechanics of bone: determinants of skeletal fragility and bone quality.

Bone fragility can be defined by biomechanical parameters, including ultimate force (a measure of strength), ultimate displacement (reciprocal of brittleness) and work to failure (energy absorption). Bone fragility is influenced by bone size, shape, architecture and tissue 'quality'. Many osteoporosis treatments build bone mass but also change tissue quality. Antiresorptive therapies, such as bisphosphonates, substantially reduce bone turnover, impairing microdamage repair and causing increased bone mineralization, which can increase the brittleness of bone. Anabolic therapies, such as parathyroid hormone (PTH-(1-84)) or teriparatide (PTH-( 1-34)), increase bone turnover and porosity, which offset some of the positive effects on bone strength. Osteoporosis therapies may also affect bone architecture by causing the redistribution of bone structure. Restructuring of bone during treatment may change bone fragility, even in the absence of drug effects on bone mineral density (BMD). This effect may explain why some drugs can affect fracture incidence disproportionately to changes in BMD. For instance, in a recent clinical trial, PTH-(1-34) therapy caused a dose-related increase in spinal BMD without any dose-dependent effect on the observed decrease in spinal fracture incidence. This apparent disassociation between spinal BMD and bone fragility is probably due to effects of PTH-(1-34) on bone architecture within vertebral bodies. While it has been shown that BMD is highly heritable, bone mineral distribution and architecture are also under strong genetic influence. Recent findings suggest that different genes regulate trabecular and cortical structures within lumbar vertebrae, producing a wide range of bone architectural designs. These findings suggest that there is no single optimal bone architecture; instead many different architectural solutions produce adequate bone strength.

Biomechanical Phenomena↗
PubMed1997

Dissociation of bone formation markers in bone metastasis of prostate cancer.

To clarify the meaning and clinical value of bone formation markers in bone metastasis from prostate cancer, we investigated the bone formation markers carboxy-terminal propeptide of type I procollagen (PICP), bone-specific alkaline phosphatase (BA1-p) and osteocalcin, so-called bone gla protein (BGP) in 43 prostate cancer patients with and 46 patients without overt bone metastasis. Patients with bone metastasis were evaluated repeatedly by bone scan at intervals of 3-6 months. The expression patterns of bone formation markers in patients with progression of bone metastasis became dissociated; BA1-p and PICP were elevated in patients with progression of bone metastasis but BGP was not. Instead, BGP showed slight elevation in patients with improvement and complete remission of bone metastasis. PICP, BA1-p and BGP are all bone formation markers, but each marker appears in a different phase of bone formation: PICP appears in proliferation phase, BA1-p appears in matrix maturation phase and BGP appears in late bone formation phase. Our findings that BGP was not elevated in progression of bone metastasis and that it increased slightly with improvement and complete remission of bone metastasis may imply that the bone formation that occurs in blastic bone metastasis is different from normal bone formation.

Aged↗