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Suppression of the osteogenic response in the aging skeleton

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Summary

The ability of physical stimuli demonstrated as potently osteogenic in the young adult skeleton were evaluated for their capacity to stimulate new bone formation in the aging skeleton. Using the externally loadable, functionally isolated turkey ulna preparation, the ulnae of 1-year-old (n=5), and 3-year-old (n=3) turkeys were subjected to 300 cycles per day of a load regimen generating a high but physiologic level of normal strain (3,000 microstrain). Following 8 weeks of loading, areal properties and histomorphometry were performed on both the experimental and intact control ulnae. Bone cross-sectional areas in the 1-year-old animal increased by 30.2% (±7.8%) as compared with the intact contralateral control ulnae, whereas the areal properties of the older skeleton remained essentially unchanged (-3.3±7.5%). Renewed bone formation in the experimental ulnae of the 1-year-old animals was characterized by the activation of periosteal bone apposition (4.0±0.4 μm/day). In comparison, periosteal bone formation in the 3-year-old males was activated in only 1 animal, and this at a significantly attenuated level (less than 0.8 μm/day). The histomorphometric evaluation of intracortical bone remodeling revealed no significant differences between the control and experimental ulnae in either age group. However, osteon mean wall thickness and bone formation sigma were significantly increased in the 3-year-old males (P<0.05). In conclusion, these data suggest that a physical signal that is clearly osteogenic in the young adult skeleton is hardly acknowledged in older bone tissue. Whether this represents a deterioration of the bone cell population's ability to perceive these physical signals or a failure of their capacity to respond is not yet clear.

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Rubin, C.T., Bain, S.D. & McLeod, K.J. Suppression of the osteogenic response in the aging skeleton. Calcif Tissue Int 50, 306–313 (1992). https://doi.org/10.1007/BF00301627

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  • DOI: https://doi.org/10.1007/BF00301627

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