Microdamage accumulation in bone has been considered a contributing cause for fragility fractures in older women and for stress fractures in athletes. Recent improvements in detecting microdamage in bone employ fluorescence and confocal microscopy, but there is still no method to detect bone microcracks noninvasively. The morphology of microcracks is characteristic of the loading mode, with linear microcracks found in regions under compressive strain, and diffuse arrays of cracks typical of regions under tensile strain. There is now good evidence that damage is associated both spatially and temporally with the initiation of bone remodeling. The detection of damage may occur by osteocytes, which signal for repair when they become apoptotic subsequent to canalicular disruption. Increased remodeling in response to damage appears to be part of the pathogenesis of stress fractures in humans. On the other hand, suppression of bone remodeling is associated with increased microdamage accumulation, reduced bone tissue toughness and increased fragility. There is evidence that the compliant bone adjacent to prosthetic implants will prevent the accumulation of microdamage, and the success rate of dental implants may be caused by the rapid turnover that maintains compliance and limits microdamage accumulation in areas juxtaposed to the implant.
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