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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 53 (1993), S. S75 
    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
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  • 2
    Publication Date: 2011-08-24
    Description: Bone is subjected in vivo to both high amplitude, low frequency strain, incurred by locomotion, and to low amplitude, broad frequency strain. The biological effects of low amplitude, broad frequency strain are poorly understood. To evaluate the effects of low amplitude strains ranging in frequency from 0 to 50 Hz on osteoblastic function, we seeded MC3T3-E1 cells into collagen gels and applied the following loading protocols for 3 min per day for either 3 or 7 days: (1) sinusoidal strain at 3 Hz, with 0-3000 microstrain peak-to-peak followed by 0.33 s resting time, (2) "broad frequency vibration" of low amplitude strain (standard deviation of 300 microstrain) including frequency components from 0 to 50 Hz, and (3) sinusoidal strain combined with broad frequency vibration (S + V). The cells were harvested on day 4 or 8. We found that the S + V stimulation significantly repressed cell proliferation by day 8. Osteocalcin mRNA was up-regulated 2.6-fold after 7 days of S + V stimulation, and MMP-9 mRNA was elevated 1.3-fold after 3 days of vibration alone. Sinusoidal stimulation alone did not affect the cell responses. No differences due to loading were observed in alkaline phosphatase activity and in mRNA levels of type I collagen, osteopontin, connexin 43, MMPs-1A, -3, -13. These results suggest that osteoblasts are more sensitive to low amplitude, broad frequency strain, and this kind of strain could sensitize osteoblasts to high amplitude, low frequency strain. This suggestion implies a potential contribution of stochastic resonance to the mechanical sensitivity of osteoblasts. Copyright 2002 Elsevier Science Ltd.
    Keywords: Aerospace Medicine
    Type: Journal of biomechanics (ISSN 0021-9290); Volume 36; 1; 73-80
    Format: text
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  • 3
    ISSN: 0021-9304
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine , Technology
    Notes: The purpose of this work is to use dynamic histomorphometry to evaluate the basic biological mechanisms by which hydroxyapatite/tricalcium phosphate (HA/TCP) implant coatings accelerate bone formation rates. Twenty-five rabbits had an HA/TCP coated cylindrical titanium fiber metal mesh implant surgically placed in the subchondral bone of the proximal tibia and a noncoated implant placed in the contralateral tibia. Twenty-two of these animals had HA/TCP coated cylindrical solid titanium implants placed in the distal femur and an uncoated implant placed in te contraleteral femur. The animals were double labeled with vital stains, and sacrificed at 3, 6, 16, or 26 weeks after surgery. Histomorphometric analyses were done of the bone implant interfaces. Both static and dynamic histomorphometric parameters indicate that HA/TCP coatings stimulate faster bone ingrowth to coated fiber metal implants through the early production of woven bone and by subsequent rapid lamellar bone formation rates. Coated fiber metal implants demonstrated significantly more bone ingrowth than noncoated implants through 16 weeks postimplatatin, but not by 26 weeks, In solid implants, the differences between coated and noncoated implants are less pronouned and not statistically significant, although there is a trend toward increased bone appostion to the surface of the implants over the first 16 weeks following implantation. The clinical significance of these results is that coated implants may allow earlier return to normal weightbearing. © 1993 John Wiley & Sons, Inc.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
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