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  • Life Sciences (General)  (3)
  • Fatigue  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Remodeling and the repair of fatigue damage (1993)
    Springer
    Calcified tissue international 53 (1993), S. S75 
    Details
    ISSN: 1432-0827
    Keywords: Microdamage ; Remodeling ; Fatigue ; Osteoporosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary This paper reviews the direct and indirect evidence for and against the idea that bone remodeling repairs fatigue damage. It defines experiments that should be performed to determine whether the accumulation and repair of fatigue damage is relevant to the pathogenesis of osteoporotic fracture. The experimental evidence favors the hypothesis that microdamage evokes local remodeling. The data suggest that the balance between the microdamage burden and bone repair is nearly constant. The indirect evidence comes from clinical observations that show positive relationships between depressed bone formation rate or prolonged remodeling period with bone fracture. More compelling indirect evidence comes from studies in which bone remodeling was pharmaceutically depressed, and fracture incidence rose in direct proportion. Data on microdamage accumulation were not collected in these studies. Conversely, some experimental evidence disputes a direct relationship between fatigue microdamage and repair. In these studies, increased amounts of bone microdamage in hyperadrenocortical dogs, and in irradiated dogs, could not be demonstrated even though bone fragility increased without associated osteopenia. Finally, the indirect evidence that argues that microdamage does not initiate repair is based on inference and does not provide an adequate test of the hypothesis. In balance, the current body of evidence favors the contention that bone remodeling repairs fatigue damage and thereby prevents fracture. Future studies should verify that microdamage accumulates when bone fracture occurs in conjunction with depressed remodeling activation frequency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01673407
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of Fatiguing Exercise on Longitudinal Bone Strain as Related to Stress Fracture in Humans (1998)
    Springer
    Annals of biomedical engineering 26 (1998), S. 660-665 
    Details
    ISSN: 1573-9686
    Keywords: Stress fracture ; Bone strain ; Fatigue ; Aging ; Exercise
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Technology
    Notes: Abstract Muscular fatigue in the training athlete or military recruit has been hypothesized to cause increased bone strain that may contribute to the development of a stress fracture. Under normal circumstances, muscles exert a protective effect by contracting to reduce bending strains on cortical bone surfaces. In vivo strain studies in dogs show that muscle fatigue following strenuous exercise elevates bone strain and changes strain distribution. However, a similar experiment has yet to be performed in humans. The purpose of this work was to test the hypothesis in humans that strenuous fatiguing exercise causes an elevation in bone strain. It was also hypothesized that this elevation is greater in younger people than in older people due to the decline in muscle strength and endurance that normally occurs with age. To test these hypotheses, strain in the tibiae of seven human volunteers was measured during walking before and after a period of fatiguing exercise. Neither hypothesis was sustained. Post-hoc analysis of the strain data suggests that strain rate increases after fatigue with a greater increase in younger as opposed to older persons. Although not conclusive, this suggests that it is strain rate, rather than strain magnitude, that may be causal for stress fracture. © 1998 Biomedical Engineering Society. PAC98: 8745Dr, 8745Bp, 0180+b
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1114/1.103
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  • 3
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    Mechanotransduction in bone: osteoblasts are more responsive to fluid forces than mechanical strain (1997)
    In:  Other Sources
    Details
    Publication Date: 2019-07-13
    Description: Mechanical force applied to bone produces two localized mechanical signals on the cell: deformation of the extracellular matrix (substrate strain) and extracellular fluid flow. To study the effects of these stimuli on osteoblasts, MC3T3-E1 cells were grown on type I collagen-coated plastic plates and subjected to four-point bending. This technique produces uniform levels of physiological strain and fluid forces on the cells. Each of these parameters can be varied independently. Osteopontin (OPN) mRNA expression was used to assess the anabolic response of MC3T3-E1 cells. When fluid forces were low, neither strain magnitude nor strain rate was correlated with OPN expression. However, higher-magnitude fluid forces significantly increased OPN message levels independently of the strain magnitude or rate. These data indicate that fluid forces, and not mechanical stretch, influence OPN expression in osteoblasts and suggest that fluid forces induced by extracellular fluid flow within the bone matrix may play an important role in bone formation in response to mechanical loading.
    Keywords: Life Sciences (General)
    Type: The American journal of physiology (ISSN 0002-9513); 273; 3 Pt 1; C810-5
    Format: text
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  • 4
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    Fluid shear-induced mechanical signaling in MC3T3-E1 osteoblasts requires cytoskeleton-integrin interactions (1998)
    In:  Other Sources
    Details
    Publication Date: 2019-07-13
    Description: Mechanical stimulation of bone induces new bone formation in vivo and increases the metabolic activity and gene expression of osteoblasts in culture. We investigated the role of the actin cytoskeleton and actin-membrane interactions in the transmission of mechanical signals leading to altered gene expression in cultured MC3T3-E1 osteoblasts. Application of fluid shear to osteoblasts caused reorganization of actin filaments into contractile stress fibers and involved recruitment of beta1-integrins and alpha-actinin to focal adhesions. Fluid shear also increased expression of two proteins linked to mechanotransduction in vivo, cyclooxygenase-2 (COX-2) and the early response gene product c-fos. Inhibition of actin stress fiber development by treatment of cells with cytochalasin D, by expression of a dominant negative form of the small GTPase Rho, or by microinjection into cells of a proteolytic fragment of alpha-actinin that inhibits alpha-actinin-mediated anchoring of actin filaments to integrins at the plasma membrane each blocked fluid-shear-induced gene expression in osteoblasts. We conclude that fluid shear-induced mechanical signaling in osteoblasts leads to increased expression of COX-2 and c-Fos through a mechanism that involves reorganization of the actin cytoskeleton. Thus Rho-mediated stress fiber formation and the alpha-actinin-dependent anchorage of stress fibers to integrins in focal adhesions may promote fluid shear-induced metabolic changes in bone cells.
    Keywords: Life Sciences (General)
    Type: The American journal of physiology (ISSN 0002-9513); 275; 6 Pt 1; C1591-601
    Format: text
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  • 5
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    Ca(2+) regulates fluid shear-induced cytoskeletal reorganization and gene expression in osteoblasts (2000)
    In:  Other Sources
    Details
    Publication Date: 2019-07-13
    Description: Osteoblasts subjected to fluid shear increase the expression of the early response gene, c-fos, and the inducible isoform of cyclooxygenase, COX-2, two proteins linked to the anabolic response of bone to mechanical stimulation, in vivo. These increases in gene expression are dependent on shear-induced actin stress fiber formation. Here, we demonstrate that MC3T3-E1 osteoblast-like cells respond to shear with a rapid increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) that we postulate is important to subsequent cellular responses to shear. To test this hypothesis, MC3T3-E1 cells were grown on glass slides coated with fibronectin and subjected to laminar fluid flow (12 dyn/cm(2)). Before application of shear, cells were treated with two Ca(2+) channel inhibitors or various blockers of intracellular Ca(2+) release for 0. 5-1 h. Although gadolinium, a mechanosensitive channel blocker, significantly reduced the [Ca(2+)](i) response, neither gadolinium nor nifedipine, an L-type channel Ca(2+) channel blocker, were able to block shear-induced stress fiber formation and increase in c-fos and COX-2 in MC3T3-E1 cells. However, 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, an intracellular Ca(2+) chelator, or thapsigargin, which empties intracellular Ca(2+) stores, completely inhibited stress fiber formation and c-fos/COX-2 production in sheared osteoblasts. Neomycin or U-73122 inhibition of phospholipase C, which mediates D-myo-inositol 1,4,5-trisphosphate (IP(3))-induced intracellular Ca(2+) release, also completely suppressed actin reorganization and c-fos/COX-2 production. Pretreatment of MC3T3-E1 cells with U-73343, the inactive isoform of U-73122, did not inhibit these shear-induced responses. These results suggest that IP(3)-mediated intracellular Ca(2+) release is required for modulating flow-induced responses in MC3T3-E1 cells.
    Keywords: Life Sciences (General)
    Type: American journal of physiology. Cell physiology (ISSN 0363-6143); 278; 5; C989-97
    Format: text
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