Biomedical Engineering Reference
In-Depth Information
Fig. 3 A backscattered scanning electron microscopy image illustrating the presence of lead-
uranyl acetate in a linear microcrack and a neighboring region with diffuse damage. Reprinted
with permission from Elsevier [ 26 ]
Alterations in microdamage with aging can result from several factors including
deterioration of bone remodeling. Remodeling of bone allows for the removal or
repair of microdamage [ 3 , 30 ]. There is strong evidence that microdamage initiates
the remodeling process for repair [ 3 , 32 ]. For instance, application of loading to
produce controlled amounts of microdamage stimulated intracortical remodeling
in rats, which typically do not remodel [ 30 , 33 ]. Microdamage can also inflict
injury to the osteocytic network or disrupt their nutritional transport, in turn
activating bone remodeling via apoptosis of osteocytes [ 34 ]. However, it has been
shown that osteocytes decrease significantly with aging and loss of osteocytes is
associated with accumulation of microdamage [ 35 ]. Hence, increasing age may
lead to accumulation of microdamage due to reduction in the ability of bone to
detect and repair damage. Recent studies have also shown that with increasing age
(or due to disease), the efficacy of the bone remodeling processes deteriorates and
thus, microdamage accumulates faster than the remodeling process can repair
these damaged areas [ 5 , 36 ].
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